Database Query Results : Magnetic Fields, ,

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy
Magnetic Fields can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range.
The main pathways affected are:
Calcium Signaling: -influence the activity of voltage-gated calcium channels.
Oxidative Stress and Reactive Oxygen Species (ROS) Pathways
Heat Shock Proteins (HSPs) and Cellular Stress Responses
Cell Proliferation and Growth Signaling: MAPK/ERK pathway.
Gene Expression and Epigenetic Modifications: NF-κB
Angiogenesis Pathways: VEGF (improving VEGF for normal cells)
PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models

Pathways:
- most reports have ROS production increasing in cancer cells , while decreasing in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, VEGF↓(mostly regulated up in normal cells),
- cause Cell cycle arrest : TumCCA↑,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDH↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF">FGF↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, cytoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Scientific Papers found: Click to Expand⟱
2612- Ba,  MF,    The effect of a static magnetic field and baicalin or baicalein interactions on amelanotic melanoma cell cultures (C32)
- in-vitro, Melanoma, NA
SOD1↑, Baicalein ONLY: increase in the expression of the SOD1 , SOD2 and GPX1 genes compared to the nontreated cell cultures
SOD2↑,
GPx1↑,
Dose?, A chamber with a field induction of 0.7 T was used for the tests
eff↝, There was no significant difference in the expression of the SOD1, SOD2 or GPX1 genes in the melanoma cell cultures that had only been exposed to a static magnetic field (0.7 T)
SOD1↓, Baicalein + 0.7T MF: decreases SOD1 , SOD2 and GPX1
SOD2↓,
GPx1↓,

2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, Capsaicin is an agonist for transient receptor potential cation channel subfamily V member 1 (TRPV1)
eff↑, It is noteworthy that capsaicin binding to the TRPV1 receptor may be increased using a static magnetic field (SMF), thus enhancing the anti-cancer effect of capsaicin on HepG2 (human hepatoblastoma cell line) cells through caspase-3 apoptosis
Akt↓, capsaicin can regulate autophagy by inhibiting the Akt/mTOR
mTOR↓,
p‑STAT3↑, Capsaicin can upregulate the activity of the signal transducer and activator of transcription 3 (p-STAT3)
MMP2↑, increase of the expression of MMP-2
ER Stress↑, capsaicin may induce apoptosis through endoplasmic reticulum (ER) stress
Ca+2↑, and the subsequent ER release of Ca2+
ROS↑, Capsaicin-induced ROS generation
selectivity↑, On the other hand, an excess of capsaicin is cytotoxic on HepG2 cells, and normal hepatocytes to a smaller extent, by collapse of the mitochondrial membrane potential with ROS formation
MMP↓,
eff↑, combination of capsaicin and sorafenib demonstrated significant anticarcinogenic properties on LM3 HCC cells, restricting tumor cell growth

659- EGCG,  MNPs,  MF,    Augmented cellular uptake of nanoparticles using tea catechins: effect of surface modification on nanoparticle-cell interaction
- in-vivo, Nor, NA
*BioEnh↑, EGCG at a concentration as low as 1-3 μM, which increased MNP uptake 2- to 7-fold. In addition, application of magnetic force further potentiated MNP uptake, suggesting a synergetic effect of EGCG and magnetic force

658- EGCG,  MNPs,  MF,    Laminin Receptor-Mediated Nanoparticle Uptake by Tumor Cells: Interplay of Epigallocatechin Gallate and Magnetic Force at Nano-Bio Interface
- in-vitro, GBM, LN229
*BioEnh↑, (EGCG), a major tea catechin, enhances cellular uptake of magnetic nanoparticles (MNPs

657- EGCG,  MNPs,  MF,    Interaction of poly-l-lysine coating and heparan sulfate proteoglycan on magnetic nanoparticle uptake by tumor cells
- in-vitro, GBM, U87MG
*BioEnh↑, enhances MNP internalization by 3.1-fold

654- EGCG,  MNPs,  MF,    Characterization of mesenchymal stem cells with augmented internalization of magnetic nanoparticles: The implication of therapeutic potential
- in-vitro, Var, NA
*BioEnh↑, (EGCG) has been known to greatly enhance MNP uptake by tumor cells

401- GoldNP,  MF,    In vitro evaluation of electroporated gold nanoparticles and extremely-low frequency electromagnetic field anticancer activity against Hep-2 laryngeal cancer cells
- in-vitro, Laryn, HEp2
Casp3↑,
P53↑,
BAX↑,
Bcl-2↓,

594- MF,  VitC,    Static Magnetic Field Effect on the Fremy's Salt-Ascorbic Acid Chemical Reaction Studied by Continuous-Wave Electron Paramagnetic Resonance
- Analysis, NA, NA
RPM↑,

537- MF,  immuno,    Integrating electromagnetic cancer stress with immunotherapy: a therapeutic paradigm
- Review, Var, NA
Apoptosis↑,
ROS↑,
TumAuto↑,
Ca+2↑, Ca++ ion tumor-cell entry
ATP↓, ATP depletion
eff↑, In physical terms, the rate of rise in a magnetic pulse or oscillation (i.e., its “sharpness”) is conveyed as dB/dt). The EMF induced by that particular period of rise to the maximum amplitude may be more impactful on unique tumor cellular features
eff↑, The induction intensity (dB/dt) may well be more critical than the field maximum amplitude (B max) in this setting

538- MF,    The extremely low frequency electromagnetic stimulation selective for cancer cells elicits growth arrest through a metabolic shift
- in-vitro, BC, MDA-MB-231 - in-vitro, Melanoma, MSTO-211H
TumCG↓, did not affect the non-malignant counterpart.
Ca+2↑,
COX2↓,
ATP↑, (ATP5B) and mitochondrial transcription (MT-ATP6)
MMP↑, significant enhancement of mitochondrial membrane potential (ΔΨm)
ROS↑, demonstrated for the first time the association of ROS production with the stimulation of the mitochondrial metabolism triggered by the electromagnetic field
OXPHOS↑,
mitResp↑, Mitochondrial respiration is increased by ELF-EMF exposure

539- MF,    Pulsed Magnetic Field Improves the Transport of Iron Oxide Nanoparticles through Cell Barriers
- in-vitro, NA, NA
eff↑, enchanced Magnetic NP uptake

582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, boost, Ascorbic acid (AA, C6H8O6) can act as an electron-donor
Ferroptosis↑, HCSVs and MF efficiently inhibited TRAMP-C1 growth through ferroptosis-mediated cell death.
ROS↑, The generated ferrous ions, inducing stronger Fenton-like oxidation than ferric ions, triggered the higher accumulation of ROS, and finally inhibited tumor cell growth
TumCG↓, Collectively, it was proved that the exogenous magnetic field-boosted Fenton reaction efficiently inhibit tumor growth.
Iron↑, after 10-min MF treatment, the increase of ferrous ions was found in 0.1 h
GPx4↓, combination treatment of MF and HCSVs downregulated GPX4

585- MF,  VitC,    Impact of pulsed magnetic field treatment on enzymatic inactivation and quality of cloudy apple juice
other↓, significant decreases of ascorbic acid were observed at the intensity of 7 T with 5–30 pulses.

587- MF,  VitC,    Effect of stationary magnetic field strengths of 150 and 200 mT on reactive oxygen species production in soybean
ROS↑,
SOD↓,
other↓, ascorbic acid content decreased

590- MF,  VitC,    Sub-millitesla magnetic field effects on the recombination reaction of flavin and ascorbic acid radicals
- in-vitro, NA, NA
RPM↑,

592- MF,  VitC,    Alternative radical pairs for cryptochrome-based magnetoreception
RPM↑,

535- MF,    Electromagnetic Fields Trigger Cell Death in Glioblastoma Cells through Increasing miR-126-5p and Intracellular Ca2+ Levels
- in-vitro, Pca, PC3 - in-vitro, GBM, A172 - in-vitro, Pca, HeLa
Apoptosis↑,
miR-129-5p↑, A172 only
Ca+2↑,
eff↝, In contrast, the cervix cancer cell line and the prostate cancer cell line remained largely unaffected.

1762- MF,  Fe,    Triggering the apoptosis of targeted human renal cancer cells by the vibration of anisotropic magnetic particles attached to the cell membrane
- in-vitro, RCC, NA
Dose∅, low frequencies (∼20 Hz) and in weak magnetic fields (∼30 mT)
Apoptosis↑, triggering of the apoptosis of these cancer cells was demonstrated with NiFe vortex particles and statistically characterized by flow-cytometry studies
Casp↑,
tumCV↓, In conclusion, a decrease of ~70% in viable cells was observed only six hours after the magneto-mechanical stimulus treatment
Casp3↑, microdisk vibrations initiated the intracellular cascade that leads to effector caspase 3/7 activation.
Casp7↑,
Ca+2↑, mechanotransduction leads to an increase of the intracellular Ca 2+ ions which serve as downstream signaling elements that propagate and amplify the apoptosis
Cyt‑c↑, The targets of such a signaling pathway include the cytochrome C release

2235- MF,    Increase of intracellular Ca2+ concentration in Listeria monocytogenes under pulsed magnetic field
- in-vitro, Inf, NA
Ca+2↑, Intracellular Ca2+ concentration in L. monocytogenes increased after PMF treatment.
TumCD↑, The death of L. monocytogenes treated by PMF might be related to the increase of intracellular Ca2+ concentration.

2236- MF,    Changes in Ca2+ release in human red blood cells under pulsed magnetic field
- in-vitro, Nor, NA
*Ca+2↓, Pulsed magnetic field (PMF) decreases Ca2+ level of inner red blood cell (RBC).
*eff↓, PMF gives RBCs positive effect consistently in Ca2+ level and plays a role in preventing RBC hemolysis from oxidative stress and improving RBCD.
*ROS↓, PMF plays a role in preventing oxidative stress or in restoring oxidative stress on RBCs.

527- MF,    Effects of Fifty-Hertz Electromagnetic Fields on Granulocytic Differentiation of ATRA-Treated Acute Promyelocytic Leukemia NB4 Cells
- in-vitro, AML, APL NB4
ROS↑, a significant increase in ROS levels was observed shortly after exposure to ELF-EMF
other↑, F-EMF exposure promotes ATRA-induced differentiation in APL NB4 cells and suggest the possible involvement of ROS and ERK signalling pathway in this phenomenon
p‑ERK↑, ERK1/2 phosphorylation
TumCP↓, ELF-EMF exposure decreases cellular proliferation potential

517- MF,  Rad,    Therapeutic Electromagnetic Field (TEMF) and gamma irradiation on human breast cancer xenograft growth, angiogenesis and metastasis
- in-vivo, NA, MDA-MB-231
TumMeta↓, IR or TEMF had significantly fewer lung metastatic sites
TumCG↓,

518- MF,    Moderate and strong static magnetic fields directly affect EGFR kinase domain orientation to inhibit cancer cell proliferation
- in-vitro, NA, HCT116
EGFR↓,
p‑EGFR↓,

519- MF,    Effects of 50-Hz magnetic field exposure on superoxide radical anion formation and HSP70 induction in human K562 cells
- in-vitro, AML, K562
HSP70/HSPA5↑, 2x

520- MF,    Exposure to a 50-Hz magnetic field induced mitochondrial permeability transition through the ROS/GSK-3β signaling pathway
- in-vitro, Nor, NA
*MPT↑, MPT induced by MF exposure was mediated through the ROS/GSK-3β signaling pathway.
*Cyt‑c↑, induced Cyt-c release
*ROS↑, cells exposed to the MF showed increased intracellular reactive oxidative species (ROS) levels and glycogen synthase kinase-3β (GSK-3β) dephosphorylation at 9 serine residue (Ser(9))
*p‑GSK‐3β↑,
*eff↓, attenuated by ROS scavenger (N-acetyl-L-cysteine, NAC) or GSK-3β inhibitor
*MMP∅, no significant effect on mitochondrial membrane potential (ΔΨm)
*BAX↓, Bax declined around 15% which was statistically significant while the total level of Bcl-2 reminded unchanged in cells
*Bcl-2∅,

521- MF,    Magnetic field effects in biology from the perspective of the radical pair mechanism
- Analysis, NA, NA
RPM↑,

523- MF,  MTX,    Extremely low-frequency magnetic fields significantly enhance the cytotoxicity of methotrexate and can reduce migration of cancer cell lines via transiently induced plasma membrane damage
- in-vitro, AML, THP1 - in-vitro, NA, PC12 - in-vivo, Cerv, HeLa
H2O2↑, These results suggest that ELF MF stimulation facilitates H2O2-dependent cell death in cancer cells as its effect was enhanced nearly two-fold
TumCD↑, 1 μM MTX
CellMemb↑,
eff↑, ELF-MF enhance the effects of methotrexate on THP-1 and PC12 cells

524- MF,    Inhibition of Angiogenesis Mediated by Extremely Low-Frequency Magnetic Fields (ELF-MFs)
- vitro+vivo, PC, MS-1 - vitro+vivo, PC, HUVECs
other↓, reduction of hemangioma size, of blood-filled spaces, and in hemorrhage.
TumCP↓,
TumCMig↓,
VEGFR2↓,
TumVol↓, 20mm compared to 32mm
HSP70/HSPA5↓, HSP70 and HSP90 expression after 72 h of exposure to MF in MS-1 cells seemed markedly reduced.
HSP90↓,
TumCCA↑, (2 mT) induced cell cycle arrest but not apoptosis. “transient” arrest of MF-treated cells in G2/M phase
angioG↓, in vitro

525- MF,    Pulsed electromagnetic fields regulate metabolic reprogramming and mitochondrial fission in endothelial cells for angiogenesis
- in-vitro, Nor, HUVECs
*angioG↑, PEMFs promoted a shift in the energy metabolism pattern of HUVECs from oxidative phosphorylation to aerobic glycolysis.
*GPx1↑, 4x
*GPx4↑, 2.2x
*SOD↑, SOD1/2 3.5x
*PFKM↑, 3x
*PFKL↑, 2.5x
*PKM2↑, 2.6x : activation of PKM2 enhanced angiogenesis in endothelial cells (ECs) by modulating glycolysis, mitochondrial fission, and fusion
*PFKP↑, 2.8x
*HK2↑, 4x
*GLUT1↑, 1.5x
*GLUT4↑, 1.6x
*ROS↓, reminder: normal HUVECs cells
*MMP↝, no damage, (normal cells)
*Glycolysis↑, (PFKL, PFKLM, PFKP, PKM2, and HK2) encoding the three key regulatory enzymes of glycolysis, hexokinase, phosphofructokinase, and pyruvate kinase, sharply increased when HUVECs were exposed to PEMFs
*OXPHOS↓, PEMFs promoted a shift in the energy metabolism pattern of HUVECs from oxidative phosphorylation to aerobic glycolysis

526- MF,    Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Pca, HeLa - vitro+vivo, Melanoma, B16-BL6 - in-vitro, Nor, HEK293
TumCG↓, Exposure to Thomas-EMF inhibited tumour growth in mice
Ca+2↑, exposure of malignant cells to Thomas-EMF for > 15 min promoted Ca2+ influx
selectivity↑, but did not effect non-malignant cells
*Ca+2∅, only malignant cells showed enhanced Ca2+ uptake following exposure to Thomas-EMF.
ROS↑, EMF-dependent increases in reactive oxygen species, rapid influx of Ca2+, or activation of specific signaling pathway
HSP70/HSPA5↑, Some studies have shown increased expression of HSP70, a marker of cellular stress responses, in response to EMF exposures
AntiCan↑, These observations suggest that the Thomas-EMF could provide a potential anti-cancer therapy.

536- MF,    Comparison of pulsed and continuous electromagnetic field generated by WPT system on human dermal and neural cells
- in-vitro, Nor, SH-SY5Y - in-vitro, GBM, T98G - in-vitro, Nor, HDFa
other∅, did not show any negative effect of the generated EMF on either normal cells or tumor cell lines

528- MF,  Caff,    Pulsed electromagnetic fields affect the intracellular calcium concentrations in human astrocytoma cells
- in-vitro, GBM, U373MG
Ca+2↑, After exposure to electromagnetic fields the basal [Ca(2+)](i) levels increased significantly from 143 +/- 46 nM to 278 +/- 125 nM
TumCP∅, Moreover the electromagnetic fields that affected [Ca(2+)](i) did not cause cell proliferation or cell death and the proliferation indexes remained unchanged after exposure.
TumCD∅,
eff↑, However, the [Ca 2+]i levels in normal and caffeine-treated cells were signicantly higher after EMF exposure than in sham exposed cells exposed cells

529- MF,    Low-frequency magnetic field therapy for glioblastoma: Current advances, mechanisms, challenges and future perspectives
- Review, GBM, NA
Ca+2↑, U-373MG 50 Hz, 3 mT 24 h Increased the intracellular Ca2+
ROS↑, BT115, U87, BT175 50–350 Hz, 1–58 mT 2–4 h Increased the ROS level and cell death
ChemoSen↑, A growing amount of evidence has validated that LF-MFs combined with chemotherapeutic drugs have a synergistic effect in the treatment of GBM
QoL↑, For example, researchers have discovered that LF-MFs can improve the quality of life of patients with recurrent GBM
OS↑, clinical trials have also validated the excellent therapeutic efficacy of LF-MFs in prolonging OS and improving quality of life in GBM patients

530- MF,    Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2
- in-vivo, Nor, NA
*miR-34b-5p↓, expression of miR-34b-5p decreased under SEMF stimulation,
*ALP↑, significant upregulation in the relative expression levels of osteogenic markers (ALP, RUNX2, BMP2, OCN, and OPN)
*RUNX2↑,
*BMP2↑,
*OCN↑,
*OPN↑,
*β-catenin/ZEB1↑, protein expression levels of osteogenic makers, including Active-β-catenin, RUNX2, and ALP, were elevated upon SEMFs exposure at 0.4 mT, 0.7 mT, and 1 mT
*STAC2↑, subsequently increasing STAC2 level.
*Diff↑, electromagnetic fields promote the osteogenic differentiation
*BMD↑, low-frequency SEMFs promote osteogenesis

531- MF,    6-mT 0-120-Hz magnetic fields differentially affect cellular ATP levels
- in-vitro, Cerv, HeLa - in-vitro, CRC, HCT116 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, Nor, RPE-1 - in-vitro, Nor, GP-293
ATP⇅, variable effects

532- MF,    A 50 Hz magnetic field influences the viability of breast cancer cells 96 h after exposure
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
TumCP↓,
MMP↓, MCF-7 breast cancer cells showed a significant decrease in ΔΨM compared with control cells after 4 and 24 h of exposure only when ΔΨM was analyzed at 96 h
ROS↑, All three breast cell lines analyzed showed an increase in ROS levels compared to those in nonexposed cells after both 4 h and 24 h of 1.0 mT ELF-MF exposure
eff↝, short-term exposure (4–8 h, 0.1 mT and 1.0 mT) led to an increase in viability in breast cancer cells, while long and high exposure (24 h, 1.0 mT) led to a decrease in viability and proliferation in all cell lines.
selectivity↑, Conversely, we did not observe significant differences in MCF-10A live cell number after 0.1 mT ELF-MF cell exposure

533- MF,    Effects of extremely low-frequency magnetic fields on human MDA-MB-231 breast cancer cells: proteomic characterization
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumCD↑,
necrosis↑, in normal MCF10A cells
mt-ROS↑, ELF-MF significantly increase the mitochondrial reactive oxygen species production in both MCF-10A and MDA-MB-231 cells, compared to the unexposed cell
other↑, ELF-MF exposed MCF-10A cells exhibited 53 upregulated and 189 downregulated proteins compared with control cells while exposed MDA-MB-231 cells showed 242 upregulated and 86 downregulated proteins compared with the control cells.
*STAT3↓, normal cells
STAT3↑, cancer cells

534- MF,    Effect of extremely low frequency electromagnetic field parameters on the proliferation of human breast cancer
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, Nor, MCF10
Ca+2↑, Exposure of the MDA-MB-231 cells to ELF-EMF also increased the fluorescence of the Ca2+ dye, FLUO-4 (AM) within 30 min, indicating an increase in Ca2+ influx compared to the control
Apoptosis↑,
eff↝, The cell viability increased with increases in the applied frequency. The ELF-EMF at 7.83Hz± 0.3 Hz showed the strongest inhibition of cell viability among the three frequency conditions
eff↑, The cells exposed to 6 h switching at 7.83Hz±0.3 Hz and 1mT for 2 consecutive days showed the strongest decrease in cell viability (from 100% to 40%)
selectivity↑, By contrast, the viability of the noncancerous M10 cells was unchanged by exposure to the T1 conditions,
eff↝, These differences in Ca2+ uptake behavior in the malignant cells could explain why MCF-7 and MDA-MB-231 cells are more sensitive than non-malignant M10 breast cells to EMF exposure.
eff↝, Our study also showed a clear window of vulnerability of cancer cells to ELF-EMF and that greater doses and magnitudes would be not unnecessarily better

2238- MF,    Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects
- Review, Var, NA
*BMD↑, Therapeutic bone-growth stimulation via Ca2+/nitric oxide/cGMP/protein kinase G. Multiple studies have implicated increased Ca2+ and nitric oxide in the EMF stimulation of bone growth
*VGCC↑, increased VGCC activity following EMF exposure and suggests, therefore, that VGCC stimulation in the plasma membrane is directly produced by EMF exposure.
*Ca+2↑, Other studies, each involving VGCCs, summarized in Table 1, also showed rapid Ca2+ increases following EMF exposure [8, 16, 17, 19, 21].
*NO↑, Multiple studies have implicated increased Ca2+ and nitric oxide in the EMF stimulation of bone growth
*eff↓, Voltage-gated calcium channel stimulation leads to increased intracellular Ca2+, which can act in turn to stimulate the two calcium/calmodulin-dependent nitric oxide synthases and increase nitric oxide.

3465- MF,    Magnetic fields and angiogenesis
- Review, Var, NA
angioG↓, angiogenesis of tumor tissues can be inhibited by both static and dynamic magnetic fields at animal level.
*angioG↑, In contrast, long-term or high-intensity static magnetic field treatment of non-tumor tissue seems to be able to promote angiogenesis at animal level.
selectivity↑,
Ca+2↝, People speculate that magnetic field may regulate angiogenesis by affecting multiple signal transduction pathways including the calcium signaling pathway.
ROS↝, studies showing that other molecules could be involved in this process, including ROS (reactive oxygen species, ROS), ERK and membrane-bound receptors

2257- MF,  HPT,    HSP70 Inhibition Synergistically Enhances the Effects of Magnetic Fluid Hyperthermia in Ovarian Cancer
- in-vitro, Ovarian, NA
eff↑, HSP70 inhibition combination with MFH generate a synergistic effect and could be a promising target to enhance MFH therapeutic outcomes in ovarian cancer.
eff↑, A significantly reduction in tumor growth rate was observed with combination therapy

2260- MF,    Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229 - in-vivo, NA, NA
TumCP↓, proliferation of human glioblastoma multiforme (GBM) cells (U87 and LN229) was inhibited upon exposure to AMF within a specific narrow frequency range, including around 227 kHz.
TumCG↓, daily exposure to AMF for 30 min over 21 days significantly suppressed tumor growth and prolonged overall survival
OS↑,
ROS↑, This effect was associated with heightened reactive oxygen species (ROS) production and increased manganese superoxide dismutase (MnSOD) expression.
SOD2↑,
eff↓, anti-cancer efficacy of AMF was diminished by either a mitochondrial complex IV inhibitor or a ROS scavenger.
ECAR↓, decrease in the extracellular acidification rate (ECAR) and an increase in the oxygen consumption rate (OCR).
OCR↑,
selectivity↑, This suggests that AMF-induced metabolic reprogramming occurs in GBM cells but not in normal cells. Furthermore, in cancer cells, AMF decreased ECAR and increased OCR, while there were no changes in normal cells.
*toxicity∅, did not affect non-cancerous human cells [normal human astrocyte (NHA), human cardiac fibroblast (HCF), human umbilical vein endothelial cells (HUVEC)].
TumVol↓, The results showed a significant treatment effect, as assessed by tumor volume, after conducting AMF treatment five times a week for 2 weeks
PGC-1α↑, Corresponding to the rise in ROS, there was also a time-dependent increase in PGC1α protein expression post-AMF exposure
OXPHOS↑, enhancing mitochondrial oxidative phosphorylation (OXPHOS), leading to increased ROS production
Glycolysis↓, metabolic mode of cancer cells to shift from glycolysis, characteristic of cancer cells, toward OXPHOS, which is more typical of normal cells.
PKM2↓, We extracted proteins that changed commonly in U87 and LN229 cells. Among the individual proteins related to metabolism, pyruvate kinase M2 (PKM2) was found to be inhibited in both.

2261- MF,    Tumor-specific inhibition with magnetic field
- in-vitro, Nor, GP-293 - in-vitro, Liver, HepG2 - in-vitro, Lung, A549
ROS↑, It enhances cell oxidative stress response and regulates apoptosis signaling pathway, changing intracellular Ca2+ concentration to induce apoptosis
Ca+2↓,
Apoptosis↑,
*selectivity↑, No signicant difference was found between the exposed 293T cell count versus the control group without magnetic exposure on the third day of exposure.
TumCG↓, Hepg2, A549 cell counts were signicantly lower than the unexposed control groups (the highest inhibition rate of Hepg2 was about 18%, and the highest inhibition rate of A549 was about 30%).
*i-Ca+2↓, Normal cells 293T showed a significant decrease in intracellular free calcium ion,
i-Ca+2↑, solid tumor cells showed no signicant change, while suspended tumor showed a slight increase in calcium ion

3457- MF,    Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis
- Review, Var, NA
Apoptosis↑, Ding et al., 8 it was demonstrated that 24‐h exposure to 60 Hz, 5 mT ELF‐EMF could potentiate apoptosis induced by H2O2 in HL‐60 leukaemia cell lines.
H2O2↑,
ROS↑, One of the main mechanisms proposed for defining anticancer effects of ELF‐EMF is induction of apoptosis through upregulation of reactive oxygen species (ROS) which has also been confirmed by different experimental studies.
eff↑, intermittent 100 Hz, 0.7 mT EMF significantly enhanced rate of apoptosis in human hepatoma cell lines pretreated with low‐dose X‐ray radiation.
eff↑, 50 Hz, 45 ± 5 mT pulsed EMF, significantly potentiated rate of apoptosis induced by cyclophosphamide and colchicine
Ca+2↑, Over the past few years, lots of data have shown that ELF‐EMF exposure regulates intracellular Ca2+ level
MAPK↑, Mitogen‐activated protein kinase (MAPK) cascades are among the other important signalling cascades which are stimulated upon exposure to ELF‐EMF in several types of examined cells
*Catalase↑, ELF‐EMF exposure can upregulate expression of different antioxidant target genes including CAT, SOD1, SOD2, GPx1 and GPx4.
*SOD1↑,
*GPx1↑,
*GPx4↑,
*NRF2↑, Activation and upregulation of Nrf2 expression, the master redox‐sensing transcription factor may be the most prominent example in this regard which has been confirmed in a Huntington's disease‐like rat model.
TumAuto↑, Activation of autophagy, ER stress, heat‐shock response and sirtuin 3 expression are among the other identified cellular stress responses to ELF‐EMF exposure
ER Stress↑,
HSPs↑,
SIRT3↑,
ChemoSen↑, Contrarily, when chemotherapy and ELF‐EMF exposure are performed simultaneously, this increase in ROS levels potentiates the oxidative stress induced by chemotherapeutic agents
UPR↑, In consequence of ER stress, cells begin to initiate UPR to counteract stressful condition.
other↑, Since the only proven effects of ELF‐EMF exposure on cells are cellular adaptive responses, ROS overproduction and intracellular calcium overload
PI3K↓, figure 3
JNK↑,
p38↑,
eff↓, ontrarily, when cells are exposed to ELF‐EMF, a new source of ROS production is introduced in cells which can at least partially reverse anticancer effects observed with cell's treatment with melatonin.
*toxicity?, More importantly, ELF‐EMF exposure to normal cells in most cases has shown to be safe and un‐harmful.

3458- MF,    Magnetic Control of Protein Expression via Magneto-mechanical Actuation of ND-PEGylated Iron Oxide Nanocubes for Cell Therapy
- in-vitro, GBM, NA
ER Stress↑, Western blot studies indicated actuated, intracellular cubic ND-PEG-SPIONs can cause mild ER stress at short periods (up to 3 h) of postmagnetic field treatment thus leading to the unfolded protein response
UPR↑,
Ca+2↑, Studies have shown that applying low-frequency magnetic fields (50 Hz) to young rats leads to stimulation of Ca2+ channel transport and therefore increases intracellular Ca2+ levels.
TRAIL↓, n the present study, we observed a similar effect where MMA caused ER stress, which resulted in a decrease in TRAIL secretion in tC17.2 stem cells
GRP78/BiP↑, A slight expression increase was also noted for the other chaperone, GRP78, for all treatment conditions.

3459- MF,    EFFECT OF PULSED ELECTROMAGNETIC FIELDS ON ENDOPLASMIC RETICULUM STRESS
- in-vitro, Cerv, HeLa
GRP78/BiP↑, the expression of BiP, Grp94 and CHOP were increased in HeLa cells upon PEMF exposure.
GRP94↑,
CHOP↑,
ER Stress↓, Our main findings are that PEMF exposure (8 Hz and meant flux density of 0.56 mT) is able to reduce the elevated activity of ER stress markers induced by tunicamycin, in HepG2 cell line.

3462- MF,    The Effect of a Static Magnetic Field on microRNA in Relation to the Regulation of the Nrf2 Signaling Pathway in a Fibroblast Cell Line That Had Been Treated with Fluoride Ions
- in-vitro, Nor, NA
*NRF2↑, Moreover, the static magnetic field had a beneficial effect on the cells with fluoride-induced oxidative stress due to stimulating the antioxidant defense.
*Keap1↓, exposure to an SMF induced a significant reduction in the level of KEAP1 mRNA compared to the untreated cells
*SOD↑, also increased activity of the antioxidant enzymes (superoxide dismutase—SOD and glutathione peroxidase—GPx) compared to the cells that had only been treated with fluoride
*GPx↑,
*ROS↓, SMF resulted in a decrease in the production of intracellular ROS and a decrease in the MDA concentration, as was shown in our previous report
*MDA↓,
*SOD1↑, SOD1, SOD2 and GSR (glutathione reductase) a significant increase in their expression was revealed in the cells that had been co-exposed to fluoride and an SMF with a 0.65 T flux density
*SOD2↑,
*GSR↑,

3463- MF,    Pulsed Electromagnetic Fields Alleviates Hepatic Oxidative Stress and Lipids Accumulation in db/db mice
- in-vivo, NA, NA
*hepatoP↑, PEMF exposure could protect the liver from oxidative stress injury by decreasing MDA and GSSG level, promoting reduced GSH level, and increasing GSH-Px activity and expression in comparison with sham group
*MDA↓,
*GSSG↓,
*GSH↑,
*GPx↑,
*antiOx↑, PEMF could increase antioxidant enzymes activity and alleviate lipid accumulation in fatty liver.
*SREBP1↓, PEMF exposure ameliorated hepatic steatosis through reducing the expression of SREBP-1c to regulate the lipid synthesis.

3464- MF,    Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology
- Review, Var, NA
AntiTum↑, frequency below 300 Hz) exert anti-tumor function, independent of thermal effects
TumCG↓, Magnetic fields (MFs) could inhibit cell growth and proliferation; induce cell cycle arrest, apoptosis, autophagy, and differentiation; regulate the immune system; and suppress angiogenesis and metastasis via various signaling pathways
TumCCA↑,
Apoptosis↑,
TumAuto↑,
Diff↑,
angioG↓,
TumMeta↓,
EPR↑, MFs not only promote the absorption of chemotherapy drugs by producing small holes on the surface of cell membrane
ChemoSen↑,
ROS↑, MF treatment has been shown to promote the generation of ROS in many studies (31, 71, 72), with exposure within a 60 Hz sinusoidal MF for 48 h in induced human prostate cancer for DU145, PC3, and LNCaP apoptoses
DNAdam↑, Repetitive exposure to LF-MFs induced DNA damage and accumulation of DSBs and triggered apoptosis in Hela and MCF7 cell lines
P53↑, PMFs could trigger apoptosis cell death by upregulating the p53 level and through the mitochondrial-dependent pathway
Akt↓, LF-MFs (300 mT, 6 Hz, 24 h) also induced apoptosis by suppressing protein kinase B (Akt) signaling, activating p38 mitogen-activated protein kinase (MAPK) signaling, and caspase-9, which is the executor of the mitochondrial apoptosis pathway
MAPK↑,
Casp9↑,
VEGFR2↓, reducing the expression and activation levels of VEGFR2
P-gp↓, A combination with the SMF (8.8 m T, 12 h) decreased the expression of P-glycoprotein (P-gp) in K562 cancer cells, while adriamycin itself induced an increase

2256- MF,  HPT,    Effects of exposure to repetitive pulsed magnetic stimulation on cell proliferation and expression of heat shock protein 70 in normal and malignant cells
- in-vitro, BC, MCF-7 - in-vitro, Cerv, HeLa - in-vitro, Nor, HBL-100
HSP70/HSPA5↑, HSP70 expression was increased by RPMS exposure under thermal stress at 40 degrees C and 42 degrees C in HBL-100 and HeLa.
HSP70/HSPA5∅, HSP70 was not affected by RPMS at 37°C (Fig. 5A).

3466- MF,    The effect of magnetic fields on tumor occurrence and progression: Recent advances
- Review, Var, NA
angioG↓, magnetic fields suppress tumor angiogenesis, microcirculation, and enhance the immune response.
ROS↝, magnetic fields suppress tumors by interfering with DNA synthesis, reactive oxygen species level, second messenger molecule delivery, and orientation of epidermal growth factor receptors.
EGFR↝,
TumCG↓, increasing evidence that MFs can inhibit tumor progression, the underlying mechanism is still poorly understood

3467- MF,    Pulsed Magnetic Field Induces Angiogenesis and Improves Cardiac Function of Surgically Induced Infarcted Myocardium in Sprague-Dawley Rats
- in-vivo, Nor, NA
*angioG↑, 15 Hz 6 mT PMF promotes myocardial angiogenesis and improves cardiac function after MI in rats.
*cardioP↑,

3468- MF,    An integrative review of pulsed electromagnetic field therapy (PEMF) and wound healing
- Review, NA, NA
*other↑, studies suggest that PEMF accelerates early stages of wound closure
*necrosis↓, By preventing necrosis, PEMF can potentially be used to reduce the incidence of ulcer formation and amputation in patients with diabetes.
*IL6↑, When gingival wounds were exposed to PEMF, one study measured an increased expression of various signalling molecules involved in proliferation including IL‑6, TGF‑β and iNOS
*TGF-β↑,
*iNOS↑,
*MMP2↑, The same study also found increased levels of MMP‑2, MCP‑1 and HO‑1 expression, all of which are thought to increase wound repair rate
*MCP1↑,
*HO-1↑,
*Inflam↓, PEMF has also been shown to reduce inflammation in chronic wounds through both intracellular and extracellular effects.
*IL1β↓, Multiple studies have measured reductions in inflammatory cytokines (IL‑1β, IL‑6, TNF‑α) following PEMF treatment
*IL6↓,
*TNF-α↓,
*BioAv↑, Electrochemotherapy mediated by PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models
eff⇅, PEMF at 50Hz, 1mT for 1 hour had increased keratinocyte proliferation compared to control groups, while the same tissue exposed to PEMF at 60Hz, 1.5mT for 144 hours had reduced cell proliferation
DNAdam↑, At higher frequencies (6–7mT), an increase in DNA double-strand breaks, apoptosis and levels of reactive oxygen species (ROS) were measured, contributing to the inhibition of cell proliferation.
Apoptosis↑,
ROS↑,
TumCP↓,
*ROS↓, tissues exposed to lower frequencies of PEMF (1mT) had decreased ROS levels
*FGF↑, Furthermore, both diabetes-related and non-diabetes-related incision wounds had similar levels of increased FGF‑2, promoting angiogenesis and preventing necrosis in response to ischaemic injury

3469- MF,    Pulsed Electromagnetic Fields (PEMF)—Physiological Response and Its Potential in Trauma Treatment
- Review, NA, NA
*eff↑, According to this analysis, pulse repetition frequencies higher than 100 Hz with magnet flux densities between 1 mT and 10 mT lead to the highest presence of a cellular response, although this may vary depending on the cell type and stage of growth
*eff↝, Also, repeated applications over a prolonged period of more than 10 days show a higher effect than shorter periods, while a prolonged acute exposure lasting more than 24 h seems to be less effective than an acute exposure with less than 24 h applicat
*other↑, release of Ca2+ ion and the direct activation of PEMF on voltage-gated calcium channels (VGCCs) is of great relevance.
Ca+2↑, PEMF stimulation also leads to similar membrane effects, resulting in a Ca2+ influx, which triggers further cellular signals
ROS↑, It has been proposed that the accumulation of ROS or oxidative stress may cause the upregulation of heat shock proteins (Hsp70, HIF-1), leading to cell damage.
HSP70/HSPA5↑,
*NOTCH↑, PEMF has been shown to increase the expressions of Notch4 and Hey1 during osteogenic differentiation of MSCs, suggesting that the Notch pathway, important in cellular fate and bone development, is activated by PEMF in stem cells
*HEY1↑,
*p38↑, PEMF-induced osteogenic differentiation MSCs, as well as the activation of p38 MAPK
*MAPK↑,

3470- MF,    Pulsed electromagnetic fields inhibit IL-37 to alleviate CD8+ T cell dysfunction and suppress cervical cancer progression
- in-vitro, Cerv, HeLa
TNF-α↑, PEMF treatment significantly inhibited IL-37 expression (p < 0.05), promoted inflammatory factor release (TNF-α and IL-6), and activated oxidative stress, leading to increased CC cell apoptosis
IL6↑,
ROS↑,
Apoptosis↑,
TumCP↓, Co-culture of Hela cells with CD8+ T cells under PEMF treatment showed reduced proliferation (by 40%), migration, and invasion (p < 0.05).
TumCMig↓,
TumCI↓,

3471- MF,    The prevention effect of pulsed electromagnetic fields treatment on senile osteoporosis in vivo via improving the inflammatory bone microenvironment
- in-vivo, Nor, NA
*BMD↑, PEMF increased the bone mineral density of the proximal femur and L5 vertebral body and improved parameters of the proximal tibia and L4 vertebral body.
*NLRP3↓, PEMF also dramatically inhibited NLRP3-mediated low-grade inflammation in the bone marrow,
*proCasp1↓, PEMF inhibited the levels of NLRP3, proCaspase1, cleaved Caspase1, IL-1β, and GSDMD-N.
*cl‑Casp1↓,
*IL1β↓,
*GSDMD↓,

3472- MF,    Pulsed electromagnetic field alleviates synovitis and inhibits the NLRP3/Caspase-1/GSDMD signaling pathway in osteoarthritis rats
- in-vivo, ostP, NA
*Inflam↓, Pulsed electromagnetic field (PEMF) can improve the symptoms of OA and potentially acts as an anti-inflammatory
*NLRP3↓, the over-expression of NLRP3, Caspase-1, and GSDMD in the cartilage of the OA rats decreased after PEMF treatment.
*Casp1↓,
*GSDMD?,

3473- MF,    Therapeutic use of pulsed electromagnetic field therapy reduces prostate volume and lower urinary tract symptoms in benign prostatic hyperplasia
- Human, BPH, NA
*Inflam↓, Pulsed electromagnetic field therapy (PEMF) (1‐50 Hz) is effective in reducing tissue inflammation.
*Dose↝, Magcell® Microcirc, Physiomed Elektromedizin AG, Scnaittach, Germany, Figure 2), with a frequency of 4‐12 Hz and an intensity of 1000 Gauss
*other?, The overall effect is a reduction in tissue hypoxia and therefore a reduction in prostatic growth

2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, PEMF-treated animals exhibited decreased glycolysis and increased LDHB expression, enhancing NAD signaling and ATP production
*LDHB↑,
*NAD↑,
*ATP↑,
*antiOx↑, Antioxidant protein levels increased, controlling ROS production.
*ROS↑,
*YAP/TEAD↑, upregulation of YAP and PGC1alpha and increasing slow myosin isoforms, thus speeding up physiological recovery.
*PGC-1α↑,
*TCA↑, increased in PEMF-treated injured limbs
*FAO↑,
*OXPHOS↑, Oxidative phosphorylation was increased in the muscle of injured rats that underwent PEMF treatment

522- MF,    Low Magnetic Field Exposure Alters Prostate Cancer Cell Properties
- in-vitro, Pca, PC3
MMP2↑, The 4 h LMF exposure caused a significant increase in MMP2 and MMP9, as well as in onco-miRs miR-155, miR-210, miR-21
MMP9↑,
miR-21↑,
miR-155↑, 57x
miR-210↑,
miR-200c↓, 1.25 fold decrease
miR-126↓, 2.5-fold decrease

2239- MF,    Time-varying magnetic fields increase cytosolic free Ca2+ in HL-60 cells
- in-vitro, AML, HL-60
Ca+2↑, cells exposed to only the time-varying magnetic field had a mean [Ca2+]i that was 34 +/- 10 nM (P less than 0.01, n = 11) higher than parallel control samples.
eff↝, Separate exposure to the radio-frequency (6.25 MHz) or static field (0.15 T) had no detectable effects.

2240- MF,    Pulsed electromagnetic field induces Ca2+-dependent osteoblastogenesis in C3H10T1/2 mesenchymal cells through the Wnt-Ca2+/Wnt-β-catenin signaling pathway
- in-vitro, Nor, C3H10T1/2
*Ca+2↑, intracellular [Ca2+]i in C3H10T1/2 cells can be upregulated upon exposure to PEMF
*Diff↑, PEMF-induced C3H10T1/2 cell differentiation was Ca2+-dependent.
*BMD↑, pro-osteogenic effect of PEMF on Ca2+-dependent osteoblast differentiation
*Wnt↑, PEMF promoted the gene expression and protein synthesis of the Wnt/β-catenin pathway.
*β-catenin/ZEB1↑, PEMF activates the Wnt/b-catenin signaling pathway in C3H10T1/2 cells
*eff↝, These data indicated that increased intranuclear [Ca2+]i resulted in altered electrical activity in the nucleus.

2241- MF,    Pulsed electromagnetic therapy in cancer treatment: Progress and outlook
- Review, Var, NA
other↝, PEMFs act on the cell, it will firstly change the cell membrane transport capacity, osmotic potential and ionic valves
p‑ERK↝, Also, it will cause changes in mitochondrial protein profile, decrease mitochondrial phosphor-ERK (extracellular-signal-regulated kinase), p53, and cytochrome c, and activate OxPhos.
P53↝,
Cyt‑c↝,
OXPHOS↑,
Apoptosis↑, PEMFs decreases cellular stress factors, increase energy demand, this series of reactions will eventually lead to apoptosis.
ROS↑, The introduction of PEFs and PEMFs can improve the penetration efficiency of ROS, not only reduce the concentration of drugs, but also reduce the irradiation dose of CAP, w

2242- MF,    Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair
- in-vitro, Nor, NA
*MMP↑, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation.
*Diff↑,
*OXPHOS↑, effect was mediated via increased OxPhos activity
*BMD↑, EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization
ATP∅, higher mitochondrial OxPhos activity leads to higher ATP production, increased cellular activity leads to increased ATP consumption.

2243- MF,    Pulsed electromagnetic fields increase osteogenetic commitment of MSCs via the mTOR pathway in TNF-α mediated inflammatory conditions: an in-vitro study
- in-vitro, Nor, NA
*eff↑, PEMF exposure increased cell proliferation and adhesion
*mTOR↑, PEMFs contribute to activation of the mTOR pathway via upregulation of the proteins AKT, MAPP kinase, and RRAGA, suggesting that activation of the mTOR pathway is required for PEMF-stimulated osteogenic differentiation.
*Akt↑,
*PKA↑, PEMFs increase the activity of certain kinases belonging to known intracellular signaling pathways, such as the protein kinase A (PKA) and the MAPK ERK1/2
*MAPK↑,
*ERK↑,
*BMP2↑, PEMFs stimulation also upregulates BMP2 expression in association with increased differentiation in mesenchymal stem cells (MSCs
*Diff↑,
*PKCδ↓, Decrease in PKC protein (involved on Adipogenesis)
*VEGF↑, Increase on VEGF (involved on angiogenesis)
*IL10↑, PEMF induced a significant increase of in vitro expression of IL-10 (that exerts anti-inflammatory activity)

2244- MF,    Little strokes fell big oaks: The use of weak magnetic fields and reactive oxygen species to fight cancer
- Review, Var, NA
RPM↑, WEMFs affect multiple cellular processes through mechanisms such as the radical pair mechanism (RPM), which alters reactive oxygen species (ROS) levels, mitochondrial function, and glycolysis
Glycolysis∅, WEMF parallel to the magnetic field (does not enchance glycolysis)
ROS↑, WEMF can augment this effect by enhancing mitochondrial respiration, which increases ROS levels within cancer cells. This augmentation makes cancer cells more susceptible to treatment by promoting oxidative stress that can lead to apoptosis
ChemoSen↑, Chemotherapeutic agents, such as doxorubicin, primarily exert their effects by generating ROS to induce cell death. WEMF can augment this effect by enhancing mitochondrial respiration, which increases ROS levels
RadioS↑, Similarly, WEMF can enhance the efficacy of radiation therapy by increasing ROS production and sensitizing cancer cells to radiation-induced DNA damage
selectivity↑, primary advantage of WEMF is its non-invasive, non-ionizing nature, which minimizes collateral damage to healthy tissue.

2245- MF,    Quantum based effects of therapeutic nuclear magnetic resonance persistently reduce glycolysis
- in-vitro, Nor, NIH-3T3
Warburg↓, tNMR might have the potential to counteract the Warburg effect known from many cancer cells which are prone to glycolysis even under aerobic conditions.
Hif1a↓, combined treatment of tNMR and hypoxia (tNMR hypoxia) led to significantly altered HIF-1α protein levels, namely a further overall reduction in protein amounts
*Hif1a∅, Under normoxic conditions we did not find significant differences in Hif-1α mRNA and protein expression
Glycolysis↓, hypoxic tNMR treatment, driving cellular metabolism to a reduced glycolysis while mitochondrial respiration is kept constant even during reoxygenation.
*lactateProd↓, tNMR reduces lactate production and decreases cellular ADP levels under normoxic conditions
*ADP:ATP↓,
Pyruv↓, Intracellular pyruvate, which was as well decreased in hypoxic control cells, appeared to be further decreased after tNMR under hypoxia
ADP:ATP↓, tNMR under hypoxia further decreased the hypoxia induced decrease of the intracellular ADP/ATP ratio
*PPP↓, pentose phosphate pathway (PPP) is throttled after tNMR treatment, while cell proliferation is enhanced
*mt-ROS↑, tNMR under hypoxia increases mitochondrial and extracellular, but reduces cytosolic ROS
*ROS↓, but reduces cytosolic ROS
RPM↑, Because EMFs are known to affect ROS levels via the radical pair mechanism (RPM)
*ECAR↓, tNMR under normoxic conditions reduces the extracellular acidification rate (ECAR)

2246- MF,    The Use of Pulsed Electromagnetic Field to Modulate Inflammation and Improve Tissue Regeneration: A Review
- in-vitro, Nor, NA
*Inflam↓, Our studies included herein confirm anti-inflammatory effects of PEMF on MSCs and MΦ
*IL1↓, PEMF significantly decreased the production of proinflammatory signaling in IL-1b, IL-6, and IL-17A cytokines (Figs. 1 and 2) in the MSCs.
*IL6↓,
IL17↓,
*TNF-α↓, After exposure to PEMF, outcomes show decreases in the proinflammatory cytokines secretion (IL-1b, IL-6, and TNF-α) and increase/stabilization of IL-10 in THP-1s (

2237- MF,    The Effect of Pulsed Electromagnetic Field Stimulation of Live Cells on Intracellular Ca2+ Dynamics Changes Notably Involving Ion Channels
- in-vitro, AML, KG-1 - in-vitro, Nor, HUVECs
Ca+2↑, In both the KG-1 and HUVECs, PEMF stimulation resulted in enhanced Ca2+ influx
selectivity↑, response of [Ca2+]i due to PEMF stimulation appeared in the opposite direction in HUVECs.
*Inflam↓, PEMF also effected a decrease in the inflammatory cytokines TNF-alpha and NFkB in macrophage-like cells [9]. Although these studies suggest that PEMF is effective in wound healing and at attenuating inflammation
*TNF-α↓,
*NF-kB↓,
*Ca+2↓, ATP-sensitive Ca2+ influx and ER Ca2+ release of HUVECs were decreased by PEMP stimulation.

2248- MF,    Magnetic fields modulate metabolism and gut microbiome in correlation with Pgc-1α expression: Follow-up to an in vitro magnetic mitohormetic study
- in-vivo, Nor, NA
*PGC-1α↑, The combination of PEMFs and exercise for 6 weeks enhanced running performance and upregulated muscular and adipose Pgc-1α transcript levels, whereas exercise alone was incapable of elevating Pgc-1α levels.
*GutMicro↑, The gut microbiome Firmicutes/Bacteroidetes ratio decreased with exercise and PEMF exposure, alone or in combination, which has been associated in published studies with an increase in lean body mass.
*FAO↓, >4 months PEMF treatment alone enhanced oxidative muscle expression, fatty acid oxidation, and reduced insulin levels.
*Insulin↓,

2249- MF,    Pulsed electromagnetic fields modulate energy metabolism during wound healing process: an in vitro model study
- in-vitro, Nor, L929
*TumCMig↑, PEMFs with specific parameter (4mT, 80 Hz) promoted cell migration and viability.
*tumCV↑,
*Glycolysis↑, PEMFs-exposed L929 cells was highly glycolytic for energy generation
*ROS↓, PEMFs enhanced intracellular acidification and maintained low level of intracellular ROS in L929 cells.
*mitResp↓, shifting from mitochondrial respiration to glycolysis
*other↝, Furthermore, the analysis of ECAR/ OCR basal ratio demonstrated a tendency toward to glycolytic phenotype in L929 cells under PEMF exposure, compared to control group
*OXPHOS↓, PEMFs promoted the transformation of energy metabolism pattern from oxidative phosphorylation to aerobic glycolysis
*pH↑, result of pH detection by flow cytometer indicated the pH level in L929 cells was significantly increased in the PEMFs group compared to the control group
*antiOx↑, PEMFs upregulated the expression of antioxidant or glycolysis related genes
*PFKM↑, Pfkm, Pfkl, Pfkp, Pkm2, Hk2, Glut1, were also significantly up-regulated in the PEMFs group
*PFKL↑,
*PKM2↑,
*HK2↑,
*GLUT1↑,
*GPx1↑, GPX1, GPX4 and Sod 1 expression were significantly higher in the PEMFs group compared to the control group
*GPx4↑,
*SOD1↑,

2250- MF,  MNPs,    Confronting stem cells with surface-modified magnetic nanoparticles and low-frequency pulsed electromagnetic field
- Review, NA, NA
*Ca+2↑, significant increase in calcium activity was observed between the 10th and 20th days of induction
*Dose↝, The average sizes of MNP, S-MNP, A-MNP and AS-MNP samples were determined as 10 ± 2 nm, 17 ± 3 nm, 14 ± 4 nm, and 18 ± 4 nm, respectively.
*BioAv↓, Several studies have shown that nanoparticles with a diameter of generally < 10 nm have been found to enter cells more easily through passive diffusion without the need for specific cellular uptake mechanisms

2251- MF,  Rad,    BEMER Electromagnetic Field Therapy Reduces Cancer Cell Radioresistance by Enhanced ROS Formation and Induced DNA Damage
- in-vitro, Lung, A549 - in-vitro, HNSCC, UTSCC15 - in-vitro, CRC, DLD1 - in-vitro, PC, MIA PaCa-2
RadioS↑, enhanced cancer cell radiosensitization associated with increased DNA double strand break numbers and higher levels of reactive oxygen species upon BEMER treatment relative to controls
DNAdam↑,
ROS↑,
ChemoSen∅, Intriguingly, exposure of cells to the BEMER EMF pattern failed to result in sensitization to chemotherapy and Cetuximab
Pyruv↓, levels of pyruvate, succinate, aspartate and adenosindiphosphate (ADP) were significantly downregulated after BEMER therapy whereas serine showed significant upregulation
ADP:ATP↓,
ROS↑, BEMER therapy increases ROS levels leading to radiosensitization via increased induction of DSBs

2252- MF,  HPT,    Cellular Response to ELF-MF and Heat: Evidence for a Common Involvement of Heat Shock Proteins?
- Review, NA, NA
HSPs∅, In some studies, no HSP-related effects were detected after ELF-MF exposure ranging from a few μT to mT and from minutes to 24 h, using different cell types such as astroglial cells (30), HL-60, H9c2, and Girardi heart cells (31, 32), and human kerat
*HSPs↑, exposure has also caused changes in HSP levels in a number of primary or non-transformed (“primary like”) cell lines.
eff↝, The hypothesis that non-stressed cells or organisms are quite responsive to HSP induction after ELF-MF exposure is strengthened by some in vivo studies in invertebrates
*eff↑, ELF-MF Exposure Potentiates the Effects of Heat on HSP Induction
eff↑, Interestingly, when HeLa and HL-60 cancer cells were subjected to comparable magnetic flux densities (10–140 µT), exposure durations (20–30 min) and concurrently heat stressed at 43°C, a stronger HSP70 expression was attained in coexposed cells
eff↓, An interesting finding is that MF exposure provides protection against heat-induced effects such as apoptosis, cell cycle disturbances, or proliferation inhibition in both cell models and in organisms

2253- MF,    Low-frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, Nor, NA
*Inflam↓, LPEMFs decreased the expression of inflammatory factors, including tumor necrosis factor-α, interleukin-1β and nuclear factor-κB.
*TNF-α↓, after 2 weeks of LPEMF treatment, the expression of TNF-α and IL-1β were decreased in comparison with the SCI group
*IL1β↓,
*NF-kB↓, administration of LPEMFs significantly reduced the immunoreactivity of NF-κB in SCI rats
*iNOS↓, Additionally, LPEMFs exposure reduced the levels of inducible nitric oxide synthase and reactive oxygen species, and upregulated the expression of catalase and superoxide dismutase.
*ROS↓, LPEMFs can alleviate the oxidative stress by reducing ROS production following SCI
Catalase↑,
*SOD↑,
*HSP70/HSPA5↑, Furthermore, treatment with LPEMFs significantly enhanced the expression of HSP70 in spinal cord-injured rats
*neuroP↑, LPEMFs exhibit strong neuroprotective effects in the nervous system
*motorD↑, LPEMF exposure can promote locomotor recovery in SCI rats
*antiOx↑, protective effect of LPEMFs on oxidative stress may be attributed to the upregulation of antioxidant enzymes.

2254- MF,    Effect of 60 Hz electromagnetic fields on the activity of hsp70 promoter: an in vivo study
- in-vivo, Nor, NA
*HSP70/HSPA5↑, induction of hsp70 (heat-shock protein 70) expression by EMFs, as well as the reporter for the luciferase gene
HSP70/HSPA5↑, We previously found activation of hsp70 promoter in cultured HeLa and BMK16 cell lines

2255- MF,    Pulsed Electromagnetic Fields Induce Skeletal Muscle Cell Repair by Sustaining the Expression of Proteins Involved in the Response to Cellular Damage and Oxidative Stress
- in-vitro, Nor, SkMC
*HSP70/HSPA5↑, HSP70), which can promote muscle recovery, inhibits apoptosis and decreases inflammation in skeletal muscle, together with thioredoxin, paraoxonase, and superoxide dismutase (SOD2), which can also promote skeletal muscle regeneration following injury
*Apoptosis↓,
*Inflam↓,
*Trx↓,
*PONs↓, Paraoxonase 2 (PON2, Paraoxonase 3 (PON3) (+19% vs. controls)
*SOD2↓,
*TumCG↑, PEMF treatment enhanced muscle cell proliferation by approximately 20% both in cells grown in complete medium
*Diff↑, suggest the potential role of PEMF in the induction of muscle differentiation
*HIF2a↑, hypoxia-inducible transcription factor 2a (HIF-2a) (+40% vs. controls),
*Cyt‑c↑, Cytochrome c (+39% vs. controls)
P21↑, p21/CIP1 (+27% vs. controls)

490- MF,    Extremely Low Frequency Magnetic Field (ELF-MF) Exposure Sensitizes SH-SY5Y Cells to the Pro-Parkinson's Disease Toxin MPP(.)
- in-vitro, Park, SH-SY5Y
ROS↑,

498- MF,    Stimulation of osteogenic differentiation in human osteoprogenitor cells by pulsed electromagnetic fields: an in vitro study
- in-vitro, NA, NA
Calcium↑,
MMP1↑, 2.8x
MMP3↑, 2.1x
BMPs↑, BMP-2 increase untill after day 9

497- MF,    In Vitro and in Vivo Study of the Effect of Osteogenic Pulsed Electromagnetic Fields on Breast and Lung Cancer Cells
- vitro+vivo, NA, MCF-7 - vitro+vivo, NA, A549
TumCG↓, growth inhibition (∼5%)
TumVol↓, 9% for PMF2
Casp3↑,
Casp7↑,
Apoptosis↑,
DNAdam↑,
TumCCA↑,
ChemoSen↑, PEMF synergistically enhances the potency of chemotherapy agents such as doxorubicin, 17 vincristine, 18 mitomycin C, 18 cisplatin, 18 and actinomycin.
EPR↑, PEMF can increase cell permeability. longer PEMF exposure may be required to increase cell membrane permeability.

496- MF,    Low-Frequency Magnetic Fields (LF-MFs) Inhibit Proliferation by Triggering Apoptosis and Altering Cell Cycle Distribution in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, ZR-75-1 - in-vitro, BC, T47D - in-vitro, BC, MDA-MB-231
ROS↑, attenuated by ROS scavenger NAC
PI3K↓,
Akt↓,
GSK‐3β↑,
Apoptosis↑,
cl‑PARP↑, cleaved PARP-1
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
CycB↓, Cyclin B1
TumCCA↑, failure of the transition from the G2 phase to M phase
p‑Akt↓,
p‑Akt↓,

495- MF,    How a High-Gradient Magnetic Field Could Affect Cell Life
- in-vitro, NA, HeLa
Apoptosis↑,
CellMemb↑, damage

494- MF,    Effects of Various Densities of 50 Hz Electromagnetic Field on Serum IL-9, IL-10, and TNF-α Levels
- in-vivo, NA, NA
IL9↓,
TNF-α↓,

493- MF,    Extremely low-frequency electromagnetic field induces acetylation of heat shock proteins and enhances protein folding
- in-vitro, NA, HEK293 - in-vitro, Liver, AML12
ATP↑,
HSP70/HSPA5↓, however, acetylations of HSP70 and HSP90 were increased
HSP90↓, however, acetylations of HSP70 and HSP90 were increased

492- MF,    Weak electromagnetic fields (50 Hz) elicit a stress response in human cells
- in-vitro, AML, HL-60
HSP70/HSPA5↑, HSP70 genes (A, B, and C), are induced by ELF-EMF

491- MF,    Pre-exposure of neuroblastoma cell line to pulsed electromagnetic field prevents H2 O2 -induced ROS production by increasing MnSOD activity
- in-vitro, neuroblastoma, SH-SY5Y
*Dose∅, 10 mins
*ROS↓, decreased reactive oxygen species production following a 30 min H2 O2 challenge

515- MF,    Pulsed Low-Frequency Magnetic Fields Induce Tumor Membrane Disruption and Altered Cell Viability
- in-vitro, Lung, A549
CellMemb↑, Induce Tumor Membrane Disruption
TumCP↓, but not that of normal lymphatic cells. ****

489- MF,    Time-varying magnetic fields of 60 Hz at 7 mT induce DNA double-strand breaks and activate DNA damage checkpoints without apoptosis
- in-vitro, NA, HeLa - in-vitro, NA, IMR90
DNAdam↑,

488- MF,    Repetitive exposure to a 60-Hz time-varying magnetic field induces DNA double-strand breaks and apoptosis in human cells
- in-vitro, NA, HeLa - in-vitro, NA, IMR90
DNAdam↑,
p‑γH2AX↑,
Chk2↑,
p38↑,
Apoptosis↑, cancer and normal cell

487- MF,    Extremely Low-Frequency Electromagnetic Fields Cause G1 Phase Arrest through the Activation of the ATM-Chk2-p21 Pathway
- in-vitro, NMSC, HaCaT
ATM↑,
Chk2↑,
P21↑,
TumCCA↑, cause G1 arrest and decrease colony formation

486- MF,    mTOR Activation by PI3K/Akt and ERK Signaling in Short ELF-EMF Exposed Human Keratinocytes
- in-vitro, Nor, HaCaT
*mTOR↑,
*PI3K↑, HaCaT cells exposed for 1h to 50Hz/1mT showed an increased percentage of cells in the S phase, through a significantly activation of the PI3K, JNK and ERK pathways
*Akt↑,
*p‑ERK↑,
*other↑, increases in the percentage of cells in the S phase and decrease in the percentage of cells in G0/G1 phase
*p‑JNK↑,
*p‑P70S6K↑,

192- MF,    The use of magnetic fields in treatment of patients with rheumatoid arthritis. Review of the literature
- Review, Arthritis, NA
*Dose↝, According Cieślińska-Świder [14], magnetic intensity of 2 mT and frequency of 12 Hz are used in arthritis. The recommended treatment time is from 15 to 30 minutes, and the treatments are performed 1–2 times per day for several weeks

194- MF,    Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke
- Review, Stroke, NA
*BAD↓,
*BAX↓,
*Casp3↓,
*Bcl-xL↑,
*p‑Akt↑,
*MMP9↓, EMF significantly decreased levels of IL-1β and MMP9 in the peri-infarct area at 24 h and 3rd day of the experiment
*p‑ERK↑, ERK1/2
*HIF-1↓,
*ROS↓, n a similar experiment, ELF-MF (50 Hz/1 mT) increased cell viability and decreased intracellular ROS/RNS in mesenchymal stem cells submitted to OGD conditions and 3 h ELF-MF exposure
*VEGF↑,
*Ca+2↓,
*SOD↑,
*IL2↑,
*p38↑,
*HSP70/HSPA5↑,
*Apoptosis↓, PEMF decreased apoptosis
*ROS↓, Nevertheless, in the presence of ischemia, EMF decreased NO and ROS concentrations.
*NO↓,

196- MF,    Mechanism for action of electromagnetic fields on cells

197- MF,    A mechanism for action of oscillating electric fields on cells

500- MF,    Anti-Oxidative and Immune Regulatory Responses of THP-1 and PBMC to Pulsed EMF Are Field-Strength Dependent
- in-vitro, AML, THP1
ROS↑, only in THP1 cells, not in normal cells ***
Prx6↑, 2x
DHCR24↑, 6x
IL10↑, 6x

514- MF,    Therapeutic electromagnetic field effects on angiogenesis and tumor growth
- in-vivo, NA, NA
TumVol↓,

513- MF,    Exposure to a specific time-varying electromagnetic field inhibits cell proliferation via cAMP and ERK signaling in cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, BC, MCF-7 - in-vivo, Pca, HeLa
TumCG↓, but did not affect non-malignant cells. ****
p‑ERK↑,
cAMP⇅, changed the level

512- MF,    Pulsed Electromagnetic Fields (PEMFs) Trigger Cell Death and Senescence in Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, FF95
TumCP↓,
*toxicity↓, PEMF application decreases the proliferation rate and viability of breast cancer cells while having the opposite effect on normal fibroblasts.
ChemoSen↑, ELF-PEMFs, as a pathology treatment approach, they have mainly been used as a complementary type of therapy, coupled with chemo-/radiotherapy,
RadioS↑,
selectivity↑, Collectively, these data indicate that PEMF irradiation exhibited not only anti-cancer properties but also beneficial effects for the normal cells.
Ca+2↑, The Thomas EMF was able to inhibit the growth of cancer cell lines including B16-BL6, MCF-7, MDA-MB-231 and HeLa via increased Ca2+ uptake through T-type Ca2+ channels but did not affect the growth of normal cells

511- MF,    Optimization of a therapeutic electromagnetic field (EMF) to retard breast cancer tumor growth and vascularity
- in-vivo, NA, NA
TumVol↓, 25% to 41%

510- MF,    Effect of a 9 mT pulsed magnetic field on C3H/Bi female mice with mammary carcinoma. A comparison between the 12 Hz and the 460 Hz frequencies
- in-vivo, NA, NA
OS↑,

509- MF,    Is extremely low frequency pulsed electromagnetic fields applicable to gliomas? A literature review of the underlying mechanisms and application of extremely low frequency pulsed electromagnetic fields
- Review, NA, NA
Ca+2↑,
TumAuto↑,
Apoptosis↑,
angioG↓,
ROS↑,

508- MF,  doxoR,    Synergistic cytotoxic effects of an extremely low-frequency electromagnetic field with doxorubicin on MCF-7 cell line
- in-vitro, BC, MCF-7
ROS↑,
Apoptosis↑,
TumCCA↑, enhanced arrest of MCF-7 cells in the G0-G1 phase

507- MF,    Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism
- in-vitro, Liver, HepG2 - in-vitro, Lung, A549 - in-vitro, Nor, GP-293
MMP↓,
TumCG↓,
ROS↑, key to tumor growth inhibition
*Ca+2↓, Normal 293 T cells showed a significant decrease in the intracellular free calcium ion concentration.
Ca+2↑, The solid tumor cells showed no significant change, while the suspended tumor cells showed a slight increase in the calcium ion concentration
selectivity↑,
i-pH↑, In addition, the intracellular pH of A549 cells increased under the magnetic field.

505- MF,    Amplitude-modulated electromagnetic fields for the treatment of cancer: Discovery of tumor-specific frequencies and assessment of a novel therapeutic approach
- Case Report, NA, NA
Pain↓, Within two weeks of experimental treatment initiation with breast cancer-specific frequencies, the patient reported complete disappearance of her pain
OS↑, two of the cases, 34mnts, and 50mnts

504- MF,    Effect of Magnetic Fields on Tumor Growth and Viability
- in-vivo, NA, NA
TumCG↓, 44x vs 500x for control (360mins only)

506- MF,  doxoR,    Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells
- in-vitro, OS, LM8
TumCP↓,
p‑CHK1↓, reducing the increased expression of total IĸB and phosphorylated-CHK1 induced by doxorubicin
Ca+2↑, caused by PEMF alone
Casp3↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
Casp7↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
p‑BAD↓,
ChemoSen↑, Our results indicate that combination of PEMF and doxorubicin could be a novel chemotherapeutic strategy.

499- MF,    The Effect of Pulsed Electromagnetic Fields on Angiogenesis
- Review, NA, NA
angioG↑, normal tissue
VEGF↑, normal tissue
VGCC↑, normal tissue

503- MF,    Effects of acute and chronic low frequency electromagnetic field exposure on PC12 cells during neuronal differentiation
- in-vitro, NA, PC12
ROS↑,
Ca+2↑,

501- MF,    Low Intensity and Frequency Pulsed Electromagnetic Fields Selectively Impair Breast Cancer Cell Viability
- in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
Apoptosis↑, MCF10 cells were slightly benefitted by these same PEMF parameters ****
*toxicity↓, harmless to non-malignant cell types
ChemoSen↑, adjuvant treatment to more traditional chemo- and radiotherapies with the aim of reducing their dosage, mitigating any harmful secondary side effects and enhancing patient prognosis.
chemoP↑,
selectivity↑, killing of MCF7 cells : 3 mT peak-to-peak magnitude, at a pulse frequency of 20 Hz and duration of exposure of only 60 minutes per day. By stark contrast, this same pulsing paradigm (cytotoxic to MCF-7s) was innocuous to normal MCF-10 breast cells
DNAdam↑, Once again, 60 minutes of 3 mT PEMFs for three consecutive days gave the greatest DNA damage in MCF7 cancer cells.

502- MF,    Electromagnetic field investigation on different cancer cell lines
- in-vitro, BC, MDA-MB-231 - in-vitro, Colon, SW480 - in-vitro, CRC, HCT116
TumCG↓, all 3 cell lines, but BC line more sensitive
Apoptosis↑,

4098- MF,    Extremely low frequency electromagnetic field (ELF-EMF) reduces oxidative stress and improves functional and psychological status in ischemic stroke patients
- Trial, Stroke, NA
*antiOx↑, Applied ELF-EMF significantly increased enzymatic antioxidant activity
*cognitive↑, ELF-EMF induced a significant improvement in functional (ADL) and mental (MMSE, GDS) status.
*Dose↝, ELF-EMF field of 40 Hz, 7 mT for 15 min/day for 4 weeks (5 days a week)

4110- MF,    Pulsed Electromagnetic Fields: A Novel Attractive Therapeutic Opportunity for Neuroprotection After Acute Cerebral Ischemia
- Review, Stroke, NA
*ROS↓, PEMFs counteract hypoxia-induced apoptosis and ROS production in neuronal-like cells and exert a strong anti-inflammatory effect on microglial cells.
*Inflam↓, PEMFs exposure is able to reduce the size of the infarct area and decrease the levels of pro-inflammatory mediators.
*other↝, Pulsed electromagnetic fields (PEMFs) act as modulators of adenosine receptors (ARs); in particular, PEMF stimulation induces a significant upregulation of A2A and A3 ARs in different cell types.
*neuroP↑, PEMFs through the specific action on A2A and A3 ARs show great potential to be exploited also to control brain inflammation and to provide neuroprotection following brain damage.
*Apoptosis↓, PEMFs exposure significantly reduced apoptosis, partially restored hypoxia inducible factor-1α (HIF-1α) activation to normoxic conditions, and inhibited ROS production.
*Hif1a↝,

4109- MF,    Overexpression of miR-26b-5p regulates the cell cycle by targeting CCND2 in GC-2 cells under exposure to extremely low frequency electromagnetic fields
- in-vitro, NA, NA
*other↝, These findings demonstrate that miR-26b-5p could serve as a potential biomarker following 50 Hz ELF-EMF exposure,

4106- MF,    Cognitive Decline: Current Intervention Strategies and Integrative Therapeutic Approaches for Alzheimer's Disease
- Review, AD, NA
*cognitive↑, Dragicevic and colleagues [52] efficiently showed that long-term exposure to high-frequency EMF treatment in Alzheimer’s transgenic (Tg) mice not only prevents cognitive impairment, but also reverses it and improves memory functioning in normal mice.
*memory↑,
*Aβ↓, EMF treatment was able to disaggregate amyloid-beta peptide (Aβ) oligomers, which are the form of Aβ that causes mitochondrial dysfunction in AD
*neuroP↑, EMF application has the capacity to selectively target microglia, eliciting neuroprotective effects against AD

4105- MF,    Extremely low frequency electromagnetic fields stimulation modulates autoimmunity and immune responses: a possible immuno-modulatory therapeutic effect in neurodegenerative diseases
- Review, AD, NA
*Inflam↓, On the basis of in vitro and clinical studies on brain activity, modulation by ELF-EMFs could possibly counteract the aberrant pro-inflammatory responses present in neurodegenerative disorders reducing their severity and their onset.
*neuroP↑, TMS (60 Hz, 0.7 mT) applied to rats for 2 hours twice daily, can be neuroprotective
*NO↑, The growth curve of exposed bacteria was lower than the control, while field application increased NO levels
*ROS↓, A significant increase of free radical production has been observed after exposure to 50 Hz electromagnetic fields at a flux density of 1 mT to mouse macrophages
*NO↓, EMF represents a non-pharmacological inhibitor of NO and an inducer of MCP-1,
*MCP1↑,
*HSP70/HSPA5↑, Tokalov and Gutzeit (2004) showed the effect of ELF-EMF on heat shock genes and demonstrated that even a low dose of ELF-EMF (10 mT) caused an increase in HSPs, especially hsp70
*antiOx↑, Whereas most environmental electromagnetic radiations cause oxidative stress in the brain (Sahin and Gumuslu, 2007), ELF-EMF seems to have an antioxidant and neuroprotective effect
*NRF2↑, ELF-EMF induces the antioxidant pathway Nrf2, which is closely associated with its protective effect against neurotoxicity induced by 3-nitropropionic acid (3-NP)
*NF-kB↓, Selective inhibition of the NF-κB signaling pathway by ELF-EMF may be involved in the decrease of chemokine production.

4104- MF,    Effects of exposure to extremely low-frequency electromagnetic fields on spatial and passive avoidance learning and memory, anxiety-like behavior and oxidative stress in male rats
- in-vivo, NA, NA
*memory↑, Our results may allow the conclusion that exposure to ELF-EMFs can improve memory retention (but not acquisition) in the adult male rats.
*ROS↑, Although exposure to ELF-EMFs could be a factor in the development of anxious state or oxidative stress.

4103- MF,    Comparing the Effects of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields With Different Values on Learning, Memory, Anxiety, and β-amyloid Deposition in Adult Rats
- in-vivo, NA, NA
*Dose↝, 1, 100, 500, and 2000 microtesla (μT), 50 Hz frequency for one h/day for two months,
*memory↑, Exposure to ELF-EMF had an anxiogenic effect on rats, promoted memory, and induced oxidative stress.
*ROS↑, exposure to the magnetic fields caused a significant increase (P<0.05) in TOS in the serum of 100, 500, and 2000 μT, compared with the control group
*MDA↑, Our results declared that the exposure to the magnetic fields caused a significant increase (P<0.05) in the levels of MDA in groups 1, 100, 500, and 2000 μT, in comparison to the control group

4102- MF,    Modulation of antioxidant enzyme gene expression by extremely low frequency electromagnetic field in post-stroke patients
- Human, Stroke, NA
*Catalase↑, We observed that after ELF-EMF therapy, the mRNA expression of the studied genes (CAT, SOD1, SOD2, GPx1, and GPx4) significantly increased, which enhanced the antioxidant defence of the body.
*SOD1↑,
*SOD2↑,
*GPx1↑,
*GPx4↑,
*Dose↝, 40 Hz frequency at 7 milliTesla, for 15 minutes per day, five days a week, over a four‑week

4101- MF,    Benign Effect of Extremely Low-Frequency Electromagnetic Field on Brain Plasticity Assessed by Nitric Oxide Metabolism during Poststroke Rehabilitation
- Human, Stroke, NA
*motorD↑, ELF-EMF treatments improved functional and mental status
*cognitive↑,
*eff↑, We conclude that ELF-EMF therapy is capable of promoting recovery in poststroke patients.
*NO↑, evidence that application of extremely low-frequency electromagnetic field increases nitric oxide generation and its metabolism, as well as improving the effectiveness of poststroke ischemic patients' treatments.
*other↝, Due to its vasodilating and proangiogenic effects, NO serves as a protective function during cerebral ischemia
*neuroP↑, In conclusion, ELF-EMF therapy increases the metabolism and generation of NO, which has both neuroprotective and cytotoxic properties.

4100- MF,    Neurobiological effects and mechanisms of magnetic fields: a review from 2000 to 2023
- Review, Var, NA
*memory↑, Alzheimer’s disease rats 50 Hz; 10 mT; 60 min/d; 14 d Improved memory
*Mood⇅, Certain conditions of MF exposure can lead to changes in emotional behavior and learning memory and cause or relieve anxiety-like and depressive behaviors, with or without significant effects.

4099- MF,    Extremely low frequency electromagnetic field reduces oxidative stress during the rehabilitation of post-acute stroke patients
- Trial, Stroke, NA
*ROS↓, all parameters of oxidative stress are significantly reduced during rehabilitation using ELF-EMF, compared to the control group rehabilitated only by kinesiotherapy

4111- MF,    Coupling of pulsed electromagnetic fields (PEMF) therapy to molecular grounds of the cell
- Review, Arthritis, NA
*Inflam↓, ultimately lead to a dampening of inflammatory signals like interleukins
*Cartilage↑, this therapy has positive effects for the regeneration of musculoskeletal tissues such as cartilage, bone, tendon and ligament
*Pain↓, Ryang We et al. [18] found a significant beneficial effect of PEMF on WOMAC pain scores at 1 month compared with a sham treatment
*QoL↑, significant improvements in mobility, daily activity score as well as global score during treatment of acute osteoarthritis of knee joint
*Dose↝, PEMF stimulation (38 Hz, 2 mT) for 2 h per day enhanced osteoblastic functions through amelioration of the cytoskeletal organization;
*VEGF↑, increase of anti-inflammatory prostaglandins, and a huge rise in the Vascular Endothelial Growth Factor (VEGF)-A-mRNA transcription.
*NO↑, stimulatory effect of PEMF on osteoblast proliferation and differentiation is accompanied by an increase in nitric oxide (NO) synthesis
*TGF-β↑, Transforming Growth Factor (TGF-β) family is enhanced by PEMF[67] and local expression of TGF-β results in improved bone fracture healing
*MMP9↓, PEMF treatment suppressed IL-1β-mediated up-regulation of MMP-9 protein levels.
*PGE2↑, Sontag and Dertinger [97] investigated the liberation of prostaglandin E2 (PGE2) during application of EMF of different frequencies: here “windows” at 6 and 16 Hz were found, where PGE was 200% above 0 Hz baseline.
*GPx3↑, PEMF exposure also induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level
*SOD2↑,
*Catalase↑,
*GSR↑,
*Ca+2↑, many EMF-effect studies is a direct action on voltage-gated calcium channels (VGCCs) (Figure 1). This is normally accompanied by a rapid increase of Ca2+

4097- MF,    Theta Frequency Electromagnetic Stimulation Enhances Functional Recovery After Stroke
- Trial, Stroke, NA
*motorD↑, ELF-EMF (5 Hz) effectively enhances functional recovery in a reach-to-grasp task, whereas neither gamma-frequency (40 Hz) nor combination frequency (5–16-40 Hz) ELF-EMFs induce a significant effect
*eff↑, gamma-band oscillations in general, and 40 Hz in specific, are important for learning and memory and for setting how the brain will form new connections as it develops.
*Dose↝, 56-turn Helmholtz coils (42 cm radius), capable of generating 1–100 Hz EMFs at intensities of 0.3 to 10G

4096- MF,    Extremely Low‐Frequency and Low‐Intensity Electromagnetic Field Technology (ELF‐EMF) Sculpts Microtubules
- in-vitro, AD, NA
*p‑tau↓, 40 Hz and 1 G Reduces Tau Phosphorylation in the Microtubule Pellet
*neuroP↑, Complementing these preconditioning neuroprotective effects, concomitant 1 h treatment protocols comparing 3.9 or 40 Hz and 1 G exposure, indicated effects on Tau phosphorylation accentuated with 40 Hz
*Dose↝, circular horizontal coil (18 cm in diameter, 50 turns of copper wire) and a waveform generator with built in amplifier (BK Precision, Yorba Linda, CA, 4045B).

4095- MF,    Frequency-tuned electromagnetic field therapy improves post-stroke motor function: A pilot randomized controlled trial
- Trial, Stroke, NA
*Dose↝, ENTF therapy (1–100 Hz, < 1 G). Participants received 40 min of active ENTF or sham treatment 5 days/week for 8 weeks;
*motorD↑, ENTF stimulation in subacute ischemic stroke patients was associated with improved UE motor function and reduced overall disability, and results support its safe use in the indicated population.

4094- MF,    EMAGINE-Study protocol of a randomized controlled trial for determining the efficacy of a frequency tuned electromagnetic field treatment in facilitating recovery within the subacute phase following ischemic stroke
- Study, Stroke, NA
*neuroP↑, low-intensity electromagnetic fields (ELF-EMF) stimulation (exposure to sham field, 3.93 Hz or 15.72 Hz, every second day, for 4 weeks) was associated in treated animals with decreased edema, increased white matter integrity, evidence of neural regen
*Dose↝, BQ 2.0; BrainQ Technologies Ltd., Jerusalem, Israel) delivers a non-invasive, extremely low-frequency (1–100 Hz) and intensity ( ≤ 1 Gauss), frequency-tuned electromagnetic field.

4093- MF,    Low-intensity electromagnetic fields induce human cryptochrome to modulate intracellular reactive oxygen species
- in-vivo, NA, NA
*ROS↑, imaging experiments that exposure of mammalian cells to weak pulsed electromagnetic fields (PEMFs) stimulates rapid accumulation of reactive oxygen species (ROS),
*eff↑, At moderate doses, we find that reactive oxygen actively stimulates cellular repair and stress response pathways, which might account for the observed therapeutic effects to repetitive magnetic stimulation.

4092- MF,    Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology
- Review, Var, NA
Apoptosis↑, 20 Hz; 3 mT, 60mins/day PEMFs increased apoptosis in MCF7 cells but had no effect on MCF10 cells
selectivity↑,
ROS↑, 50 Hz, 0.1–1.0 mT) for 30 min, and long‐term PEMF: undifferentiated PC12 cells increased ROS levels and decreased catalase activity
Catalase↓,
TumVol↓, 1 Hz, 100 mT, Mice exposed for 60 and 180 min daily showed a 30% and 70% tumor reduction
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies

4015- MF,    Evaluation of the PTEN and circRNA-CDR1as Gene Expression Changes in Gastric Cancer and Normal Cell Lines Following the Exposure to Weak and Moderate 50 Hz Electromagnetic Fields
- in-vitro, GC, AGS - in-vitro, Nor, HU02
*PTEN↑, We have found that the activity of PTEN gene in the normal and tumor cells increased and decreased with increasing intensity of discontinuous electromagnetic field, respectively.
PTEN↓,
Dose↝, in general, the effect of electromagnetic field on gastric cancer seems to depend on the kind of exposure as well as an extent of intensity and can be used for cancer therapeutic purposes.

3942- MF,    Chronic-Exposure Low-Frequency Magnetic Fields (Magnetotherapy and Magnetic Stimulation) Influence Serum Serotonin Concentrations in Patients with Low Back Pain-Clinical Observation Study
- Human, AD, NA
*5HT↑, Magnetotherapy and magnetic stimulation, acting in a similar way, increase the concentration of serotonin.

3746- MF,    Low-Frequency Pulsed Electromagnetic Field Is Able to Modulate miRNAs in an Experimental Cell Model of Alzheimer's Disease
- in-vitro, AD, NA
*cognitive↑, EMFs could protect from the cognitive impairment or improve the memory in mice [9
*memory↑,
*BACE↓, figure 2

3744- MF,    Cognitive improvement via a modulated rhythmic pulsed magnetic field in D-galactose-induced accelerated aging mice
- in-vivo, AD, NA
*cognitive↑, enhancement in spatial learning and memory abilities upon PMF stimulation of the accelerated aging mice.
*memory↑,

4150- MF,    Enhanced effect of combining bone marrow mesenchymal stem cells (BMMSCs) and pulsed electromagnetic fields (PEMF) to promote recovery after spinal cord injury in mice
- in-vitro, NA, NA
*BDNF↑, PEMF promoted the expression levels of BDNF and VEGF in BMMSCs via Wnt/β‐catenin signaling pathway.
*VEGF↑,

4568- MF,    Extremely low-frequency pulses of faint magnetic field induce mitophagy to rejuvenate mitochondria
- Study, NA, NA
*ETC↓, We report that ELF-WMF efficiently suppresses the mitochondrial mass to 70% by inhibiting the mitochondrial ETC complex II, which subsequently induces mitophagy and rejuvenates mitochondria.
*OCR↑, We found that Opti-ELF-WMF increased both the OCR and mitochondrial membrane potential by approximately 40%
*MMP↑,
*ROS⇅, Opti-ELF-WMF most strongly decreased the level of mitochondrial superoxide at 1 h, mitochondrial mass at 3 h, and mitochondrial membrane potential at 6 h, and most strongly increased them at 12 h
*MMP⇅,

4425- MF,  doxoR,    Brief Magnetic Field Exposure Stimulates Doxorubicin Uptake into Breast Cancer Cells in Association with TRPC1 Expression: A Precision Oncology Methodology to Enhance Chemotherapeutic Outcome
- in-vitro, BC, 4T1 - in-vitro, BC, MCF-7
ChemoSen↑, PEMF therapy may enhance DOX cytotoxicity in breast cancer cells,
TRPC1↑, increased by TRPC1 overexpression,
Dose↓, PEMF exposure enhances DOX-mediated killing of breast cancer cells, reducing the IC50 value of DOX by half, whereas muscle cells, representative of collateral tissues, were less sensitive to PEMF-enhanced DOX-mediated cytotoxicity
selectivity↑, whereas muscle cells, representative of collateral tissues, were less sensitive to PEMF-enhanced DOX-mediated cytotoxicity.

4356- MF,    Pulsed electromagnetic fields synergize with graphene to enhance dental pulp stem cell-derived neurogenesis by selectively targeting TRPC1 channels
- in-vitro, Nor, NA
*Diff↑, brief PEMF exposure promotes in vitro differentiation by activating a TRPC1-mitochondrial axis
*TRPC1↑,
*ROS↑, PEMF-stimulated neurogenic induction of hDPSCs through their mutual capacity to activate TRPC1with subsequent ROS production.

4355- MF,    Ambient and supplemental magnetic fields promote myogenesis via a TRPC1-mitochondrial axis: evidence of a magnetic mitohormetic mechanism
- in-vitro, Nor, C2C12
*mt-OCR↑, figure 1
*mt-ROS↑, Exposure to PEMFs stimulated the production of ROS (Fig. 6A, B) and ATP
*ECAR↑, figure 6
*Dose↝, barrages of 20 × 150 μs on and off pulses for 6 ms repeated at a frequency of 15 Hz. The magnetic flux density rose to predetermined maximal level within ∼50 μs (∼17 T/s) when driving field amplitudes between 0.5 and 3 mT.
*Ca+2↑, 10 min) of C2C12 myoblasts to PEMFs (Supplemental Fig. S1A) augmented cytosolic calcium levels [intracellular [Ca2+] concentration ([Ca2+]i), blue] relative to unexposed myoblasts
*ATP↑,
*other↑, PEMF-stimulated proliferation of myoblasts
*eff↓, TRPC1 silencing precludes PEMF sensitivity.
*eff↝, revealed a magnetic efficacy window

4354- MF,  doxoR,    Modulated TRPC1 Expression Predicts Sensitivity of Breast Cancer to Doxorubicin and Magnetic Field Therapy: Segue Towards a Precision Medicine Approach
- in-vivo, BC, MDA-MB-231 - in-vivo, BC, MCF-7
selectivity↑, PEMF exposure alone impaired the survival of MCF-7 and MDA-MB-231 cells, but not that of non-malignant MCF10A breast cells; the selective vulnerability of breast cancer cells to PEMF exposure was corroborated in human tumor biopsy samples
Apoptosis↑,
TumCI↓, PEMF exposure was shown to attenuate the invasiveness of MCF-7 cells in correlation with TRPC1 expression
tumCV↓, PEMF exposure was previously shown to impair the viability of MCF-7 breast cancer cells when administered at an amplitude of 3 mT for 1 h per day
TumVol↓, PEMF treatment alone significantly reduced tumor volume by ~-20%
eff↓, Notably, stronger PEMF exposures (5 mT) were ineffective at killing MCF-7 and MDA-MB-231 breast cancer cells
eff↑, PEMF and DOX treatments hence synergize in vitro to slow breast cancer cell growth.
ROS↑, figure 4. PEMF exposure stimulates ROS production in cancer (29, 30) and non-cancer (5, 31, 32) cells.
Ca+2↑, PEMF exposure (blue) consistently increased cytoplasmic calcium over baseline (red) and was further augmented with increasing DOX concentration
TumCMig↓, PEMF Exposure Slows the Migration and Decreases the Invasiveness of TRPC1-Overexpressing Breast Cancer Cells

4353- MF,  Chemo,    Pulsed Electromagnetic Field Enhances Doxorubicin-induced Reduction in the Viability of MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF-7
TumCCA↑, PEMF enhances the anticancer activity in DOX-treated MCF-7 breast cancer cells by increasing G1 cell cycle arrest and caspase-dependent apoptosis.
Apoptosis↑, we report that PEMF stimulation enhances the reduction in the cell viability by enhancing cell cycle arrest and apoptosis in MCF-7 breast cancer cells.
eff↑, extremely low frequency (ELF)-EMF can increase the cytotoxic effect of DOX on MCF-7 breast cancer cells compared with treatment with DOX alone
TumCCA↑, we report here that PEMF enhances DOX-induced cell cycle arrest in G1 phase and caspase-dependent apoptosis
Casp↝, PEMF promoted the DOX-induced activation of caspases-8, -9, and -7
p‑CDK2↓, combined treatment with DOX and PEMF produced the further reduction in CDK2 phosphorylation and cyclin E2 expression when compared to treatment with DOX alone
cycE↓,
Fas↑, expression of Fas and Bax was elevated to a larger degree in the DOX/PEMF-treated cells than in the DOX-treated cells
BAX↑,
survivin↓, expression of survivin was decreased in the DOX-treated cells and further reduced in the DOX/PEMF-treated cells
Mcl-1↓, Mcl-1 expression was reduced in the DOX/PEMF-treated cells compared to the DOX-treated cells
cl‑PARP↑, increased PARP cleavage was observed in the DOX/PEMF-treated cells
cl‑Casp7↑, caspase-7 was higher in the DOX-treated cells than in the control group and was further higher in the DOX/PEMF-treated cells
cl‑Casp8↑, Cleavage of caspase-8 and -9 were elevated in the DOX-treated cells and increased even more in the DOX/PEMF-treated cells
cl‑Casp9↑,

4352- MF,    Differences in lethality between cancer cells and human lymphocytes caused by LF-electromagnetic fields
- in-vitro, lymphoma, K562 - NA, NA, U937 - NA, NA, HL-60
Apoptosis↑, Similar apoptosis and necrosis can be obtained using moderate magnetic fields (B < or = 15 mT 50/60 Hz), but this requires longer treatment of at least over a week.
eff↑, PEMF application combined with anticancer drugs and photodynamic therapy will be very effective.

4351- MF,    Inhibition of proliferation of human lymphoma cells U937 by a 50 Hz electromagnetic field
- in-vitro, lymphoma, NA
Apoptosis↑, Fields > or =3.5 mT treatment kill > or =80% of the cell number at the beginning (1.5 x 10(5)/ml).

4349- MF,    Long-term effect of full-body pulsed electromagnetic field and exercise protocol in the treatment of men with osteopenia or osteoporosis: A randomized placebo-controlled trial
- Trial, ostP, NA
*BMD↑, The BMD of total hip and lumbar spine was significantly increased post-treatment in all groups
*Pain↓, PEMFs also help patients with osteoporosis feel better by reducing pain, improving functional results and improving quality of life (QoL)
*QoL↑,
*toxicity↓, PEMF therapy has gained extensive use due to its quick effects, ease of use, and lack of side effects
*Dose↝, 30 min/day, with intensity 100%, and frequency 5-15 Hz, three times/week.
*Inflam↓, PEMFs have a considerable anti-inflammatory and analgesic effect on the joint environment (Varani et al., 2017).

4348- MF,    Pulsed electromagnetic field attenuates bone fragility in estrogen-deficient osteoporosis in rats
- in-vivo, ostP, NA
*BMD↑, The application of PEMF40Hz, significantly reduced the osteoporotic bone loss in female rats

3742- MF,    The role of magnetic fields in neurodegenerative diseases
- Review, AD, NA - Review, Park, NA
cognitive↑, other authors reported that exposure to electromagnetic fields was beneficial in both mouse and rat models of AD

4149- MF,    Pulsed Electro-Magnetic Field (PEMF) Effect on Bone Healing in Animal Models: A Review of Its Efficacy Related to Different Type of Damage
- Review, NA, NA
*other↑, The expression of placental growth factor (PlGF) was significantly higher in the PEMF-treated group compared to the expression level before PEMF treatment.
*BDNF↑, Other factors trended higher following active PEMF treatment including BDNF and BMP-7 and -5.
*BMPs↑,
*BMD↑, PEMF accelerated bone regeneration, resulting in increased BV and BMD in groups that received 0, 2.5, and 5 μg rhBMP-2.

4148- MF,    Increase in Blood Levels of Growth Factors Involved in the Neuroplasticity Process by Using an Extremely Low Frequency Electromagnetic Field in Post-stroke Patients
- Human, Stroke, NA
*neuroP↑, We observed that ELF-EMF significantly increased growth factors and cytokine levels involved in neuroplasticity, as well as promoted an enhancement of functional recovery in post-stroke patients.
*BDNF↑, The increase of the BDNF level in the ELF-EMF group was about 200%
*Dose↝, magnetic induction of 5 mT, 40 Hz, rectangular and bipolar waveforms) was conducted in the ELF-EMF group

4147- MF,    PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration
- in-vitro, AD, PC12
*ROS↓, PEMF treatment significantly counteracted H2O2- and Aβ-induced cytotoxicity by restoring cell viability, reducing reactive oxygen species production, and improving catalase activity.
*Catalase↑,
*MMP↑, PEMFs preserved the mitochondrial membrane potential and decreased caspase-3 activation and chromatin condensation
*Casp3↓,
*p‑ERK↓, Mechanistically, PEMFs inhibited ERK phosphorylation and enhanced cAMP levels, CREB phosphorylation, and BDNF expression
*cAMP↑,
*p‑CREB↑,
*BDNF↑,
*neuroP↑, PEMFs modulate multiple stress response systems, promoting neuroprotection under oxidative and amyloidogenic conditions.

4146- MF,    Pulsed electromagnetic field enhances brain-derived neurotrophic factor expression through L-type voltage-gated calcium channel- and Erk-dependent signaling pathways in neonatal rat dorsal root ganglion neurons
- in-vivo, AD, NA
*BDNF↑, Exposure to 50Hz and 1mT PEMF for 2h increased the level of [Ca(2+)]i and Bdnf mRNA expression
*ERK↑, indicating that Erk activation is required for PEMF-induced upregulation of BDNF expression.

4120- MF,    Low-Frequency Repetitive Transcranial Magnetic Stimulation of the Right Dorsolateral Prefrontal Cortex Enhances Recognition Memory in Alzheimer's Disease
- Human, AD, NA
*memory↑, Right real rTMS significantly improved memory performance compared to right sham rTMS (p = 0.001).

4119- MF,    Therapeutic potential and mechanisms of repetitive transcranial magnetic stimulation in Alzheimer’s disease: a literature review
- Review, AD, NA
*cognitive↑, Recent clinical evidence demonstrates that rTMS can significantly improve cognitive function, memory, language abilities, and motor performance in AD patients, particularly when administered with optimized parameters targeting key brain regions, such
*memory↑,
*motorD↑,
*eff↑, Meta-analyses indicate that high-frequency protocols (particularly 20 Hz) delivered over at least 3 weeks with a minimum of 20 sessions produce the most significant cognitive improvements
*eff↑, high-frequency stimulation at 20 Hz, with stimulation durations of 1–2 s and intervals of 20–30 s between stimulations
*Dose↝, The common scheme of intermittent θ burst is 2 s burst, 8 s off, and repeated in turn
*Dose↝, After half an hour of transcranial magnetic stimulation treatment with 1.5 T
*Dose↝, rTMS to the left dorsolateral prefrontal cortex (DLPFC) at 120% of motor threshold, using 10 Hz frequency for 4-s durations, with 26-s intervals between train deliveries, totaling 75 trains (37.5 min per session).
*BDNF↑, repetitive transcranial magnetic stimulation reverses hippocampal depletion of nerve growth factor and brain-derived neurotrophic factor (BDNF)
*Aβ↓, reduces β-amyloid (Aβ) aggregation—mechanisms that collectively improve cognitive function.
*eff↑, Studies have identified 3 Hz as the optimal stimulation frequency for achieving maximal therapeutic benefit in addressing swallowing disorders

4118- MF,    Effects of transcranial magnetic stimulation on neurobiological changes in Alzheimer's disease
- Review, AD, NA
*cognitive↑, TMS may increase brain cortical excitability, induce specific potentiation phenomena, and promote synaptic plasticity and recovery of impaired functions; thus, it may re-establish cognitive performance in patients with AD.
*BDNF↑, Notably, a number of studies have indicated an increase in endogenous neurotrophic content (BDNF) in the affected brain regions after TMS therapy
*neuroP↑, neuroprotective and neuroregenerative effects
*memory↑, 1 Hz LF-rTMS: reversed memory deficits, and improved spatial memory retrieval ability.
*ROS↓, 20 Hz HF-rTMS: Increased visual recognition memory functions, decreased oxidant status, increased anti-oxidant levels and improvement in familiarity-based cognition.
*antiOx↑,
*Aβ↓, Repeated electromagnetic field stimulation (3 mT; 75 Hz) Decreased Aβ toxicity
*eff↑, TMS parameters combined with short trains and long inter-train intervals carry a lower risk of side effects

4117- MF,    Pulsed electromagnetic fields improve the healing process of Achilles tendinopathy: a pilot study in a rat model
- in-vivo, NA, NA
*other↑, daily exposure to PEMFs generally provided an improvement in the fibre organization, a decrease in cell density, vascularity, and fat deposition, and a restoration of the physiological cell morphology compared to untreated tendons.

4116- MF,    Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, NA, NA
*Inflam↓, LPEMFs decreased the expression of inflammatory factors, including tumor necrosis factor-α, interleukin-1β and nuclear factor-κB.
*TNF-α↓,
*IL1β↓,
*iNOS↓, LPEMFs exposure reduced the levels of inducible nitric oxide synthase and reactive oxygen species, and upregulated the expression of catalase and superoxide dismutase.
*ROS↓,
*Catalase↑,
*SOD↑,
HSP70/HSPA5↑, treatment with LPEMFs significantly enhanced the expression of HSP70 in spinal cord-injured rats.

4112- MF,    Novel protective effects of pulsed electromagnetic field ischemia/reperfusion injury rats
- in-vivo, Stroke, NA
*cardioP↑, in vivo results showed that per-treatment of PEMF could significantly improve the cardiac function in I/R injury group
*Bcl-2↑, up-regulating the expression of anti-apoptosis protein B-cell lymphoma 2 (Bcl-2) and down-regulating the expression of pro-apoptosis protein (Bax)
*BAX↓,
*ROS↓, PEMF treatment could significantly reduce the apoptosis and reactive oxygen species (ROS) levels in primary neonatal rat cardiac ventricular myocytes (NRCMs) induced by hypoxia/reoxygenation (H/R)

3482- MF,    Pulsed Electromagnetic Fields Increase Angiogenesis and Improve Cardiac Function After Myocardial Ischemia in Mice
- in-vitro, NA, NA
*cardioP↑, PEMF treatment with 30 Hz 3.0 mT significantly improved heart function.
*VEGF↑, PEMF treatment with 15 Hz 1.5 mT and 30 Hz 3.0 mT both increased capillary density, decreased infarction area size, increased the protein expression of vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR2
*VEGFR2↑,
*Hif1a↑, and increased the mRNA level of VEGF and hypoxia inducible factor 1-alpha (HIF-1α) in the infarct border zone.
*FGF↑, Additionally, treatment with 30 Hz 3.0 mT also increased protein and mRNA level of fibroblast growth factor 2 (FGF2), and protein level of β1 integrin, and shows a stronger therapeutic effect.
*ITGB1↑,
*angioG↑, PEMFs Improve Angiogenesis In Vivo

3501- MF,    Unveiling the Power of Magnetic-Driven Regenerative Medicine: Bone Regeneration and Functional Reconstruction
- Review, NA, NA
*VEGF↑, Releasing VEGF under magnetic stimulation;
*BMPs↓, sinusoidal EMF promotes osteogenic differentiation of BMSCs by up-regulating the gene expression of BMP receptors (BMPR1A, BMPR1B, and BMPR2) and associated signaling components (Smad4 and Smad1/5/8) (
*SMAD4↑,
*SMAD5↑,
*Ca+2↑, PEMFs cause Ca2+ influx in MSCs and stimulate them through pathways such as Wnt/β-catenin and BMP, thereby promoting their osteogenic differentiation.

3500- MF,    Moderate Static Magnet Fields Suppress Ovarian Cancer Metastasis via ROS-Mediated Oxidative Stress
- in-vitro, Ovarian, SKOV3
ROS↑, SMFs increased the oxidative stress level and reduced the stemness of ovarian cancer cells.
CSCs↓,
CD44↓, xpressions of stemness-related genes were significantly decreased, including hyaluronan receptor (CD44), SRY-box transcription factor 2 (Sox2), and cell myc proto-oncogene protein (C-myc).
SOX2↓,
cMyc↓,
TumMeta↓, High Levels of Cellular ROS Inhibit Ovarian Cancer Cell Migration and Invasion
TumCI↓,
TumCMig↓, Moderate SMFs Increase Ovarian Cancer Cell ROS Levels and Inhibit Cell Migration
CD133↓, stemness-related genes were significantly downregulated by SMF treatment, including Sox2, Nanog, C-myc, CD44, and CD133
Nanog↓,

3474- MF,    Pulsed electromagnetic fields potentiate the paracrine function of mesenchymal stem cells for cartilage regeneration
- in-vitro, Nor, NA
*Inflam↓, PEMF-induced CM was capable of enhancing the migration of chondrocytes and MSCs as well as mitigating cellular inflammation and apoptosis.
*Apoptosis↓,
*other↑, modulating the paracrine function of MSCs for the enhancement and re-establishment of cartilage regeneration in states of cellular stress.
*PGE2↓, studies showing PEMF inhibition of the PGE2 and cycloxigenase-2 (COX-2) pathways, reducing the expression of pro-inflammatory cytokines (IL-6, IL-8) while augmenting anti-inflammatory factors (cAMP, IL-10) in synovial fibroblasts from bovine and ost
*COX2↓,
*IL6↓,
*IL8↓,
*cAMP↑,
*IL10↑,

3487- MF,  Rad,    High-specificity protection against radiation-induced bone loss by a pulsed electromagnetic field
- Review, Var, NA
radioP↑, A unique pulsed-burst EMF (PEMF) at 15 Hz and 2 mT induces notable Ca2+ oscillations with robust Ca2+ spikes in osteoblasts in contrast to other waveforms. This waveform parameter substantially inhibits radiotherapy-induced bone loss
*Ca+2↑,
RAS↑, PEMF-induced activation of Ras/MAPK signaling.
MAPK↓,

3486- MF,    Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death
- in-vitro, NA, NA
ChemoSen↑, It is established that pulsed electromagnetic field (PEMF) therapy can enhance the effects of anti-cancer chemotherapeutic agents
tumCV↓, co-treatment with etoposide and PEMFs led to a decrease in viable cells compared with cells solely treated with etoposide.
cl‑PARP↑, PEMFs elevated the etoposide-induced PARP cleavage and caspase-7/9 activation and enhanced the etoposide-induced down-regulation of survivin and up-regulation of Bax.
Casp7↑,
Casp9↑,
survivin↓,
BAX↑,
DNAdam↑, PEMF also increased the etoposide-induced activation of DNA damage-related molecules
ROS↑, the reactive oxygen species (ROS) level was slightly elevated during etoposide treatment and significantly increased during co-treatment with etoposide and PEMF.
eff↓, Moreover, treatment with ROS scavenger restored the PEMF-induced decrease in cell viability in etoposide-treated MCF-7 cells

3485- MF,    Cytoprotective effects of low-frequency pulsed electromagnetic field against oxidative stress in glioblastoma cells
- in-vitro, GBM, U87MG
*antiOx↑, The cytoprotective effect of PEMF against deleterious effects of oxidative stress triggered by different time interval of H2O2 treatment might be mediated by the increase in the cell viability, the elevation in the antioxidant enzyme activity/amount,
*ROS↓,
*cytoP↑,

3484- MF,    Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
- in-vitro, Nor, NA
*GPx↑, ELF-PEMF exposure induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level.
*SOD2↑,
*Catalase↑,
*GSR↑,
*ROS↓, After 5 and 6 exposures (days 4 and 7) DCF fluorescence (ROS levels) was even decreased (−14.5% and −26.5% respectively) compared to untreated hOBs

3483- MF,    Pulsed Electromagnetic Fields Protect Against Brain Ischemia by Modulating the Astrocytic Cholinergic Anti-inflammatory Pathway
- NA, Stroke, NA
*Inflam↓, PEMF exposure reduced the activation of astrocytes and neuroinflammation following brain ischemia by directly modulating astrocytic injury and inflammatory cytokine release.
*STAT3↓, negative regulation of signal transducer and activator of transcription 3 (STAT3) by α7nAChR was found to be an important downstream mechanism through which PEMF regulates astrocyte-related neuroinflammation.
*p‑STAT3↓, PEMF suppressed STAT3 phosphorylation and nuclear translocation by activating α7nAChR.

3498- MF,    Effect of Static Magnetic Field on Oxidant/Antioxidant Parameters in Cancerous and Noncancerous Human Gastric Tissues
- in-vitro, GC, NA
*SOD↑, SMF causes increase in SOD activity and decrease in MDA level in the noncancerous tissue.
*MDA↓,
SOD↓, However, it decreases SOD and glutathione peroxidase (GSH-Px) activities and increases MDA level and catalase (CAT) activity in the cancerous tissue.
GPx↓,
MDA↑,
Catalase↑,

3481- MF,    No effects of pulsed electromagnetic fields on expression of cell adhesion molecules (integrin, CD44) and matrix metalloproteinase-2/9 in osteosarcoma cell lines
- in-vitro, OS, MG63 - in-vitro, OS, SaOS2
ITGA1∅, PEMF exposure on the expression levels of some metastasis-related molecules, including integrin α subunits (α1, α2, α3, α4, α5, α6, αv), integrin β subunits (β1, β2, β3, β4), CD44, and (MMP-2/9) in 4 human osteosarcoma
ITGB1∅,
ITGA5∅,
ITGB3∅,
ITGB4∅,
MMP2∅,
MMP9∅,
eff↑, PEMF exposure has no effect on the expression of some molecules that are associated with tumor cell invasion and metastasis, and therefore suggest that PEMF exposure may be safely applied to chemotherapy for osteosarcoma.

3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, NA, NA
ROS↑, 50 Hz, 1 mT for 24/48/72 h SH-SY5Y (neuroblastoma Significantly increased ROS levels
*Ca+2↑, There is experimental proof that extremely low-frequency (ELF-MF) magnetic fields interact with Ca2+ channels, leading to increased Ca2+ efflux
*Inflam↓, PEMF stimulates the anti-inflammatory response of mesenchymal stem cells.
*Akt↓, nasopharyngeal carcinoma cell line. Potentially, these alterations were caused by inhibition of the Akt/mTOR signaling pathway
*mTOR↓,
selectivity↑, Ashdown and colleagues observed disruptions in the human lung cancer cell line after PMF (20 mT) exposure; in comparison, normal cells were insensitive to PMF
*memory↑, Ahmed and colleagues proved that PMF has an impact on the hippocampus, the brain region responsible for spatial orientation and memory acquisition.
*MMPs↑, In wound closure, epithelial cells, connective tissue cells, and immune cells, which promote collagen production, matrix metalloproteinase activity, growth factor release (e.g., VEGF, FGF, PDGF, TNF, HGF, and IL-1), and inflammatory environment pro
*VEGF↑,
*FGF↑,
*PDGF↑,
*TNF-α↑,
*HGF/c-Met↑,
*IL1↑,

3479- MF,    Evaluation of Pulsed Electromagnetic Field Effects: A Systematic Review and Meta-Analysis on Highlights of Two Decades of Research In Vitro Studies
- Review, NA, NA
*eff↓, evidence suggests that frequencies higher than 100 Hz, flux densities between 1 and 10 mT, and chronic exposure more than 10 days would be more effective in establishing a cellular response
eff↝, undifferentiated PC12 cells are more sensitive to PEMF exposure, while differentiated PC12 cells are more resistant to stress
*Hif1a↑, Retinal pigment epithelial (RPE) cells Frequency of 50 Hz Intensity of 1 mT : HIF-1α, VEGFA, VEGFR-2, CTGF, cathepsin D TIMP-1, E2F3, MMP-2, and MMP-9) increased
*VEGF↑,
*TIMP1↑,
*E2Fs↑,
*MMP2↑,
*MMP9↑,
Apoptosis↑, MCF7, MCF10 Frequencies of 20 and 50 Hz Intensities of 2.0, 3.0, and 5.0 mT Cell apoptosis

3478- MF,    One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study
- Trial, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, C2C12
TumCP↓, Female sera from the magnetic therapy group (n = 12) reduced breast cancer cell proliferation (16.1%), migration (11.8%) and invasion (28.2%) and reduced the levels of key EMT markers relative to the control sera
TumCMig↓,
TumCI↓,
*toxicity∅, The provision of week 5 or week 8 PEMF sera to MCF10A cells did not alter their viability, being comparable to that observed with the control sera (
TGF-β↓, The week 8 PEMF sera resulted in the significant downregulation of (A) TGFβR2, (B) TWIST, (C) SNAI1, (D) SNAI2 (Slug), (E) β-catenin and (F) Vimentin protein expressions, when compared to week 8 control sera
Twist↓,
Slug↓,
β-catenin/ZEB1↓,
Vim↓,
p‑SMAD2↓, Week 5 PEMF sera primarily reduced the phosphorylation of SMAD 2/3 as well as the expression of TWIST protein expression.
p‑SMAD3↓,
angioG↓, Week 8 PEMF-plasma showed significant reductions in angiogenic biomarkers, including Angiopoietin-2, BMP-9, Endoglin, PLGF, VEGF-A, and VEGF-D
VEGF↓,
selectivity↑, PEMF sera did not adversely alter the growth of non-malignant cells such as MCF10A (breast epithelial) and C2C12 (myogenic).
LIF↑, Similarly, LIF (leukemia inhibitory factor) was upregulated one week after the final PEMF treatment.

3477- MF,    Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis
- Review, NA, NA
*Ca+2↑, When cells are subjected to external mechanical stimulation, voltage-gated ion channels in the cell membrane open and intracellular calcium ion concentration rises
*VEGF↑, BMSCs EMF combined with VEGF promote osteogenesis and angiogenesis
*angioG↑,
Ca+2↑, 1 Hz/100 mT MC4-L2 breast cancer cells EMF lead to calcium ion overload and ROS increased, resulting in necroptosis
ROS↑,
Necroptosis↑,
TumCCA↑, 50 Hz/4.5 mT 786-O cells ELF-EMF induce G0/G1 arrest and apoptosis in cells lines
Apoptosis↑,
*ATP↑, causing the ATP or ADP increases, and the purinergic signal can upregulate the expression of P2Y1 receptors
*FAK↑, Our research team [53] found that ELE-EMF can induce calcium oscillations in bone marrow stem cells, up-regulated calcium ion activates FAK pathway, cytoskeleton enhancement, and migration ability of stem cells in vitro is enhanced.
*Wnt↑, ability of EMF to activate the Wnt10b/β-catenin signaling pathway to promote osteogenic differentiation of cells depends on the functional integrity of primary cilia in osteoblasts.
*β-catenin/ZEB1↑,
*ROS↑, we hypothesize that the electromagnetic field-mediated calcium ion oscillations, which causes a small amount of ROS production in mitochondria, regulates the chondrogenic differentiation of cells, but further studies are needed
p38↑, RF-EMF was able to suppress tumor stem cells by activating the CAMKII/p38 MAPK signaling pathway after inducing calcium ion oscillation and by inhibiting the β-catenin/HMGA2 signaling pathway
MAPK↑,
β-catenin/ZEB1↓,
CSCs↓, Interestingly, the effect of electromagnetic fields is not limited to tumor stem cells, but also inhibits the proliferation and development of tumor cells
TumCP↓,
ROS↑, breast cancer cell lines exposed to ELE-EMF for 24 h showed a significant increase in intracellular ROS expression and an increased sensitivity to further radiotherapy
RadioS↑,
Ca+2↑, after exposure to higher intensity EMF radiation, showed a significant increase in intracellular calcium ion and reactive oxygen species, which eventually led to necroptosis
eff↓, while this programmed necrosis of tumor cells was able to be antagonized by the calcium blocker verapamil or the free radical scavenger n -acetylcysteine
NO↑, EMF can regulate multiple ions in cells, and calcium ion play a key role [92, 130], calcium ion acts as a second messenger that can activate downstream molecules such as NO, ROS

3476- MF,    Pulsed Electromagnetic Fields Stimulate HIF-1α-Independent VEGF Release in 1321N1 Human Astrocytes Protecting Neuron-like SH-SY5Y Cells from Oxygen-Glucose Deprivation
- in-vitro, Stroke, 1321N1 - in-vitro, Park, NA
*VEGF↑, PEMF exposure induced a time-dependent, HIF-1α-independent release of VEGF from 1321N1 cells
*eff↑, further corroborate their therapeutic potential in cerebral ischemia.
*neuroP↑, emerging evidence has identified PEMFs as an attractive non-invasive strategy also for the treatment of different neuropathological conditions
*other↑, PEMF stimulation have been studied in the context of Parkinson’s disease [2,3], Alzheimer’s disease [4], and neuropathic pain
*eff↑, PEMFs significantly reduced neuroinflammation and pro-apoptotic factors and determined a reduction of infarct size, implicating PEMFs as possible adjunctive therapy for stroke patients
*Inflam↓, anti-inflammatory effect of PEMFs in microglial cells
*Hif1a∅, PEMFs exposure did not modulate HIF-1α expression confirming that the PEMF-mediated VEGF production was independent by the activation of this transcriptional regulator of cellular response to hypoxia

3475- MF,    A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells
- in-vitro, Nor, HT22 - Review, AD, NA
*Apoptosis↓, PEMF exposure improved viability of HT22 cells after excitotoxicity and reduced lactate dehydrogenase release and cell death.
*LDH↓,
*neuroP↑, PEMF exposure indicated that the neuroprotective effects of PEMF were related to modulation of the eCB metabolic system.
*toxicity∅, Recent studies have shown that PEMF is a safe and non-invasive approach for management of several neurological diseases, including Alzheimer's disease
*IL1β↓, Previous studies have shown that PEMF could modulate inflammation after traumatic brain injury by inhibiting production of pro-inflammatory factor IL-1β
*Inflam↓, PEMF influences neuroinflammation via elevation of anti-inflammatory IL-10 and reduction of pro-apoptotic tumor necrosis factor
*IL10↑,
*TNF-α↓,

3735- MF,    Examining the effects of extremely low-frequency magnetic fields on cognitive functions and functional brain markers in aged mice
- in-vivo, AD, NA
*APP∅, No difference in hippocampal expression of APP-695, Aβ(1−42), S100b and GFAP proteins or in the pTau/Tau ratio was observed between sham- and ELF-MF-exposed aged mice
*Aβ∅,
*Inflam∅, ELF-MFs does not aggravate aging and associated neuroinflammation, or promote pathological pathways involved in the initiation of AD
*memory∅, However, sham- and ELF-MF-exposed aged mice were equally able to discriminate the newly accessible arm during the test phase, which resulted in a spatial recognition memory performance above chance level

3724- MF,  RF,    Electromagnetic Field in Alzheimer's Disease: A Literature Review of Recent Preclinical and Clinical Studies
- Review, AD, NA
*memory↑, recent evidence revealed that exposure to electromagnetic fields (EMF) can delay the development of AD and improve memory.
*neuroP↑,

3569- MF,    Current Evidence Using Pulsed Electromagnetic Fields in Osteoarthritis: A Systematic Review
- Review, Arthritis, NA
*Pain↓, Pain reduction, assessed through VAS and WOMAC scores, showed significant improvement (60% decrease in VAS, 42% improvement in WOMAC). The treatment duration varied (15 to 90 days), with diverse PEMF devices used
*QoL↑, Secondary outcomes included improvements in quality of life, reduced medication usage, and enhanced physical function.
*motorD↑,

3536- MF,    Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis
- Review, Arthritis, NA - Review, Stroke, NA
*Inflam↓, (PEMF), a biophysical form of stimulation, has an anti-inflammatory effect by causing differentiation of MSCs.
*Diff↑,
*toxicity∅, PEMF have been reported to last up to 3 months or longer in human patients with chronic inflammatory/autoimmune disorders (38) with no evidence of adverse effects (39).
*other↑, MSCs to promote immunomodulation and improve cartilage and bone regeneration in vitro (10) and in vivo (73).
*SOX9↑, enhanced chondrogenic gene expression in SOX-9, COL II, and aggrecan in MSCs
*COL2A1↑,
*NO↓, Prevented increases in NO
*PGE2↓, Exposure to PEMF induces early upregulation of adenosine receptors A2A and A3 that reduce PGE2 and pro-inflammatory cytokines such as TNF-α, which combine to inhibit the activation of transcription factor NF-kB
*NF-kB↓,
*TNF-α↓, 1 h exposure to PEMF has been shown to down-regulate both NF-kB and TNF-α in murine macrophages
*IL1β↓, By inhibiting NF-kB activation (94), exposure to PEMF led to decreased production of TNF-α, IL-1β, IL-6, and PGE2 in human chondrocytes, osteoblasts, and synovial fibroblasts
*IL6↓,
*IL10↑, Inhibited release of PGE2, and IL-1β and IL-6 production, while stimulating release of IL-10 in synovial fibroblasts
*angioG↑, progenitor cells (EPCs) to an RA injury site is important for repair of vasculature and angiogenesis. PEMF has also been reported to increase the number and function of circulating EPCs in treating myocardial ischemia/reperfusion (I/R) injury in rat
*MSCs↑, Since PEMF have been shown to stimulate the production of MSCs
*VEGF↑, promoting the expression of growth factors such as VEGF and TGF-β
*TGF-β↑,
*angioG↝, modulate the aberrant angiogenesis present in RA: reported to significantly reduce activation levels of VEGF (15), to inhibit the proliferative ability of HUVECs, and to reduce the extent of vascularization in diseased tissue
*VEGF↓, diseased tissue
Ca+2↝, By restoring normal Ca2+ ion flux and Na+/K+ balance, the cell can begin the process of down-regulating inflammatory cytokines, HSPs, and proangiogenic molecules such as VEGF, making it possible for the body to commence rebuilding healthy cartilage.

3725- MF,    Short-term effects of extremely low frequency electromagnetic fields exposure on Alzheimer's disease in rats
- in-vivo, AD, NA
*Weight∅, body weight of rats showed no difference compared with the control group.
*memory∅, application of ELF-EMF did not induce any cognitive and memory impairment compared with the sham-exposure group.
*cognitive∅,
*Aβ∅, Aβ showed no significant change between the two groups,

3726- MF,    Spatial memory recovery in Alzheimer's rat model by electromagnetic field exposure
- in-vivo, AD, NA
*memory↑, ELF-MF improved the learning and memory impairments in Aβ injection+M and AD+M groups.
*cognitive↑, Our results showed that application of ELF-MF not only has improving effect on different cognitive disorder signs of AD animals, but also disrupts the processes of AD rat model formation.

3727- MF,    RKIP-Mediated NF-κB Signaling is involved in ELF-MF-mediated improvement in AD rat
- in-vivo, AD, NA
*cognitive↑, ELF-MF exposure partially improved the cognitive disorder, upregulated the levels of RKIP, TAK1, and the RKIP/TAK1 interaction, but downregulated p-IKK levels in AD rats
*RKIP↑, RKIP was significantly increased in the AD+MF group (P = 0.017) compared with the AD group at 14 d after ELF-MF exposure.
*p‑IKKα↓, downregulated at 7 d in the AD+MF group compared with both the Con group

3728- MF,    Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice
- in-vivo, AD, NA
*cognitive↑, ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice.
*neuroP↑, protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice.
*Apoptosis↓,
*ROS↓,
*p‑tau↓, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac.
*GSK‐3β↓,
*CDK5↓,

3734- MF,    Extremely low frequency electromagnetic fields promote cognitive function and hippocampal neurogenesis of rats with cerebral ischemia
- in-vivo, AD, NA
*cognitive↑, rats treated with ELF-EMF required shorter swimming distances and latencies in the Morris water maze test than those of untreated rats.
*NOTCH1↑, Up-regulation in the expressions of Notch1, Hes1, and Hes5 proteins, which are the key factors of the Notch signaling pathway, was greatest in the treated rats.

3737- MF,    The Effect of Time-Dependence of 10 Hz Electromagnetic Field on Spatial Learning and Memory in Rats
- in-vivo, AD, NA
*memory↑, ELF-EMF affects spatial learning and memory and can improve memory, especially with long-term exposure.
*BDNF↑, radiation for 30 days resulted in a substantial rise in BDNF levels.
*BBB↑,

3739- MF,    Early intervention using long-term rhythmic pulsed magnetic stimulation alleviates cognitive decline in a 5xFAD mouse model of Alzheimer's disease
- in-vivo, AD, NA
*memory↑, exhibiting improved learning and memory abilities.
*cognitive↑,
*Aβ↓, cPMF exposure alleviated Aβ plaque deposition and astrogliosis in the AD brain.
*FGF↑, neurotrophic factor fibroblast growth factor 1 (FGF1) in the AD brain was upregulated by cPMF treatment.

3568- MF,    The Efficacy of Pulsed Electromagnetic Fields on Pain, Stiffness, and Physical Function in Osteoarthritis: A Systematic Review and Meta-Analysis
- Review, Arthritis, NA
*eff↑, Compared with the control groups, the PEMF treatment yielded a more favorable output.
*Pain↓, PEMF alleviated pain (standardized mean differences [SMD] = 0.71, 95% confidence interval [CI]: 0.08–1.34, p = 0.03),
*motorD↑, improved stiffness (SMD = 1.34, 95% CI: 0.45–2.23,p=0.003), and restored physical function (SMD = 1.52, 95% CI: 0.49–2.55,p=0.004).

3740- MF,    Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, DMS treatment enhances cognitive performances, attenuates Aβ load, upregulates postsynaptic density protein 95 level, and promotes hippocampal long-term potentiation in 5XFAD mouse brain.
*Dose↝, Successive trains of DMS for 40 minutes were administered daily for continuous 8 weeks.
*Aβ↓, When DMS was administered, the average area occupied by Aβ positive plaques was decreased in 5XFAD mice.
*PSD95↑, DMS could restore PSD95 expression in the brain of 5XFAD mice

3566- MF,    Positive and Negative Effects of Administering a Magnetic Field to Patients with Rheumatoid Arthritis (RA)
- Study, Arthritis, NA
*Inflam↓, Magnetotherapy applied to patients with rheumatoid arthritis (RA) produces anti-inflammatory, analgesic and antioedema effects.
*QoL↑, findings show improved functional status by 0.26 points on average (p = 0.0166) measured with the Health Assessment Questionnaire (HAQ-20),
*Pain↓, reduced pain by 2.2 points on average (p = 0.0000) on the Visual Analogue Scale (VAS)
*motorD↑, decreased duration of morning stiffness by 23.2 min on average (p = 0.0010) and reduced severity of morning stiffness by 15.2 points on average. entire group showed an increase in the range of motion in the joints of the dominant hand by 1.9 mm on av
*toxicity↓, Magnetotherapy, being a non-thermal method, is safe and rarely causes negative effects
*Cartilage↑, it slows down degenerative processes in the porcine articular cartilage.
*Inflam↓, Conversely, in the PEMF group, the hand volume decreased by as much as 19.5 mm3 on average and the change was statistically significant.

3741- MF,    Promising application of Pulsed Electromagnetic Fields (PEMFs) in musculoskeletal disorders
- Review, NA, NA
*eff↑, effectively treat numerous musculoskeletal disorders, such as delayed union or nonunion fractures, osteoarthritis (OA), osteoporosis (OP), osteonecrosis (ON), tendon disorders, etc.
*BMD↑, n 1964, Bassett et al. [8] demonstrated the effects of electric currents on new bone growth in vivo
*Inflam↓, arani et al. also demonstrated the PEMFs exerted a strong anti-inflammatory effect on the joint environment via acting as agonist of A2A and A3 adenosine receptors [
*PGE2↓, The receptor activation can reduce the release of prostaglandin E2 (PGE2) and pro-inflammatory cytokines IL-6 and IL-8, as well as inhibit the activation of the transcription factor NF-KB
*IL6↓,
*IL8↓,
*NF-kB↓,
*mTOR↝, mTOR) pathway has also been demonstrated to be the underlying signaling pathway of PEMFs involved in bone formation

3488- MFrot,  MF,    Rotating magnetic field improves cognitive and memory impairments in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway
- in-vivo, AD, NA
*cognitive↑, RMF treatment significantly ameliorated their cognitive and memory impairments, attenuated neuronal damage, and reduced amyloid deposition.
*memory↑,
*neuroP↑,
*Aβ↓,
*PI3K↓, RMF improves cognitive and memory dysfunction in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway, thus highlighting the potential of RMF as a clinical treatment for hereditary AD.
*Akt↓,
*mTOR↓,

3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,

3489- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer's disease mice.
- in-vivo, AD, NA
*Aβ↓, RMF directly inhibited Aβ amyloid fibril formation and reduced Aβ-induced cytotoxicity in neural cells .
*motorD↑, RMF restored motor abilities to healthy control levels and significantly alleviated cognitive impairments, including exploration and spatial and non-spatial memory abilities.
*cognitive↑,
*memory↑,
*ROS↓, reduced oxidative stress in the APP/PS1 mouse brain.

3491- MFrot,  MF,    Magnetically controlled cyclic microscale deformation of in vitro cancer invasion models
- in-vitro, BC, MDA-MB-231
Ca+2↑, Intracellular calcium influx was observed in response to cyclic actuation, as well as an influence on cancer cell invasion from 3D spheroids, as compared to unactuated controls.
ATF3↑, 15 fold increase, fig 6
FOSB↑,

3492- MFrot,  Chemo,  MF,    Synergistic Effect of Chemotherapy and Magnetomechanical Actuation of Fe-Cr-Nb-B Magnetic Particles on Cancer Cells
eff↑, efficient cancer cell destruction by exploiting the magnetomechanical actuation (MMA) of Fe-Cr-Nb-B magnetic particles (MPs), which are loaded with clinically approved chemotherapeutic drugs.
TumCD↑, The parallelepipedic shape grants magnetic shape anisotropy to the particles, resulting in a significant rotational torque in the rotating magnetic field, which leads to the destruction of cancer cells.

3493- MFrot,  MF,    Mechanical nanosurgery of chemoresistant glioblastoma using magnetically controlled carbon nanotubes
- in-vivo, GBM, NA
TumCD↑, We show that GBM cells internalize mCNTs, the mobilization of which by rotating magnetic field results in cell death.
MMP↓, We detected the dissipation of mitochondria membrane potential of GBM cells upon mCNT + magnetic treatment
Cyt‑c↑, When mitochondria integrity is compromised, mitochondrial cytochrome C is released into the cytosol to initiate caspases-dependent apoptosis
Apoptosis↑,
OS↑, Consistent with tumor burden reduction, mCNT + magnetic field treatment significantly extended the survival of GBM-bearing mice (median survival: 22.2 ± 4.0 versus 26.8 ± 6.0 days, P = 0.0072; Fig. 3F).
DNAdam↑, Tumor cells in the treatment group also exhibited increased DNA damage

3494- MFrot,  MF,    Magnetically switchable mechano-chemotherapy for enhancing the death of tumour cells by overcoming drug-resistance
- in-vitro, Var, NA
eff↑, RMF exposure induces a mechanical movement to this nanomaterial, which can be exploited for (i) controllably releasing the anti-cancer drug for chemotherapy,
TumCD↑, (ii) promoting the death of tumour cells by means of mechanical forces exerted onto their membranes

3495- MFrot,  MF,    Synthesis of urchin-like nickel nanoparticles with enhanced rotating magnetic field-induced cell necrosis and tumor inhibition
- in-vivo, BC, NA
TumCG↓, UNNPs showed obvious suppression against tumor cell growth in a mouse model of malignant breast cancer under the induction of low-frequency RMF.

3496- MFrot,  GoldNP,  MF,    Enhancement of chemotherapy effects by non-lethal magneto-mechanical actuation of gold-coated magnetic nanoparticles
- in-vitro, Cerv, HeLa
eff↑, Here, we show how the MMA method based on magnetically-rotated gold-coated MNP boosts only the activity of an unbound antitumor drug, without physical damage of cells via MNP
tumCV↓, Au@MNP particles, slightly rotated by an external magnetic field, manages to be significantly more effective in decreasing tumor cell viability compared to chemotherapy alone.

3497- MFrot,  MF,    The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets
- Human, Nor, NA
*PDGFR-BB↑, The highest concentration of PDGF-BB was observed in the samples placed in RMF for 1 h at 25 Hz
*TGF-β↑, For TGF-β1, the highest concentrations were obtained in the samples exposed to RMF for 3 h at 25 Hz and 1 h at 50 Hz.
*IGF-1↑, highest concentrations of IGF-1 and FGF-1 were shown in plasma placed in RMF for 3 h at 25 Hz.
*FGF↑,
*angioG↑, Magnetic fields have been shown to have a beneficial effect on vasodilation, angiogenesis, accelerating repair, regeneration, and healing of soft tissues, nervous tissues and bones, analgesic aspects, anti-swelling, reducing inflammation and pain, an
*Inflam↓,
*ROS↓, RMF exposure can increase resistance to heat stress, reduce levels of ROS, affect intracellular calcium ion concentrations, and contribute to cell aging deceleration

3499- MFrot,  MF,    Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans
- in-vitro, Nor, HUVECs
*AntiAge↑, RMF exposure prolonged the lifespan of C. elegans and slowed the aging of HUVECs
*AMPK↑, RMF treatment of HUVECs showed that activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) was associated with decreased mitochondrial membrane potential (MMP) due to increased intracellular Ca2+ concentrations induced by endo
*mPGES-1↓,
*Ca+2↑,
*ER Stress↑,
*OS↑, prolonged lifespan of C. elegans was associated with decreased levels of daf-16 which related to the insulin/insulin-like growth factor signaling pathway (IIS) activity and reactive oxygen species (ROS),
*ROS↓,

3567- MFrot,  MF,    The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review
- Review, Stroke, NA
*eff↑, All included studies showed a beneficial effect of ELF-MFs on stroke patients
*ROS↓, Improvements were observed in domains such as oxidative stress, inflammation, ischemic lesion size, functional status, depressive symptoms and cognitive abilities.
*Inflam↓,
*cognitive↑, An improvement in cognitive abilities reported in some of the included studies [25,26,27,28] is in line with other researchers’ finding
*Catalase↑, Cichoń et al. [27] also showed that catalase activity in erythrocytes and superoxide dismutase were significantly higher in the experimental group than in the control group.
*SOD↑,
*SOD1↑, similar effect was observed in regard to SOD1 and SOD2 mRNA levels.
*SOD2↑,
*GPx1↑, ELF-MFs impacted also the expression of GPx1 and GPx4 mRNA, which increased in the experimental group about 160% (p < 0.001) and 140% (p < 0.001), respectively.
*GPx4↑,
*IL1β↑, blood samples of IL-1β in the experimental group after 10 sessions of rehabilitation which involved ELF-MFs were significantly higher than in the control group
*neuroP↑, majority of the articles included in this study, a neuroprotective effect of ELF-MFs was indicated
*toxicity∅, Particularly noteworthy is the fact that none of the studies included in this review reported any negative side effects of ELF-MFs.

3535- MFrot,  MF,    Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications
- Review, Nor, NA
*eff↑, Pulsed electromagnetic fields (PEMFs) are currently used as a safe and non-invasive treatment to enhance bone healing and to provide joint protection.
*COL2A1↑, exposure to PEMFs induced increased collagen type II (Col2) expression and glycosaminoglycan (GAG) content
*SOX9↑, PEMFs significantly increased the expression of chondrogenic genes (SOX9, collagen type II, and aggrecan) and the deposition of cartilaginous matrix (sulphated GAG)
*Ca+2↑, Intracellular Ca2+ increase
*FAK↑, FAK activation
*F-actin↑, increased F-actin network formation
*Inflam↓, anti-inflammatory effect of PEMFs exposure has been extensively described above
*other↑, PEMFs exert a strong anti-inflammatory effect protecting cartilage tissue from the catabolic activity of pro-inflammatory cytokines.
*Diff↑, commonly recognized that PEMFs exposure induces osteogenic differentiation of MSCs
*BMD↑, Emerging evidence shows that PEMFs stimulation represents a safe non-invasive approach to favor bone repair and optimize bone tissue engineering

2258- MFrot,  MF,    EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE
- in-vitro, GBM, GBM - in-vitro, Nor, SVGp12
TumVol↓, GBM patient reversed the progression of his recurrent tumor causing >30% reduction in its contrast-enhanced volume within 4 weeks of treatment
OS↑, Mice with implanted mouse glioma cells in their brains also showed marked reduction in tumor size, increased survival (p< 0.05, n = 10)
γH2AX↑, higher DNA damage (g-H2AX foci) after sOMF treatment with a whole-body stimulation method developed by us
DNAdam↑,
selectivity↑, Normal mice exposed to sOMF for 4 months had no adverse effects on the brain and other organs
ROS↑, sOMF markedly increased reactive oxygen species (ROS) levels in cancer cells leading to the selective death of these cells, while sparing normal neurons and astrocytes
TumCD↑,
eff↑, sOMF exposure for just 2 h resulted in >40% loss of surviving GBM and DIPG cell colonies detected by clonogenic cell survival assay, similar to that produced by 2 Gy radiation dose.
eff↓, This loss was rescued by the antioxidant Trolox

2311- MFrot,  MF,    Magnetic fields as a potential therapy for diabetic wounds based on animal experiments and clinical trials
- in-vivo, Nor, HaCaT
*COX2↓, ELF‐EMF exposure enhances the proliferation of keratinocyte HaCaT cells and improves early NOS activity, while decreases cyclooxygenase 2 (COX‐2) which indicates its role in accelerating the transition from inflammation phase to remodelling phase.
*Inflam↓,
*MMP9↑, Exposure to ELF‐EMF with frequency of 50 Hz and intensity of 1 mT increases cytokine release and activates the expression of MMP‐9 in human immortalized keratinocytes
*GPx↑, On the contrary, ELF‐EMF activates glutathione peroxidase with decrease in malondialdehyde in the live tissue of rats during wound healing process
*Diff↑, ELF‐EMF promotes the proliferation and differentiation of transplanted epidermal stem cells in the full‐thickness defect nude mice

2262- MFrot,  MF,    Effects of 0.4 T Rotating Magnetic Field Exposure on Density, Strength, Calcium and Metabolism of Rat Thigh Bones
- in-vivo, ostP, NA
*BMD↑, strong magnetic field (MF) exposure could effectively increase bone density and might be used to treat osteoporosis
*eff↓, calcium supplement tended to increase the indexes of thigh bone density, energy absorption, maximum load, maximum flexibility, and elastic deformation
*ALP↑, alkaline phosphatase (ALP), serum phosphate, and serum calcium were higher in rats exposed to RMF with calcium
*other↑, RMF is in fact capable of increasing density, strength, calcium, and metabolism in bones

201- MFrot,  MF,    Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vitro, BC, MDA-MB-468
CCDC150↓, magnetic field response gene
TGF-β↓,
SMAD3↓,

202- MFrot,  MF,    Systematic simulation of tumor cell invasion and migration in response to time-varying rotating magnetic field
- Analysis, Var, MDA-MB-231
TumCG↓, inhibit tumor progression
MMPs↓,
ECM/TCF↓,

2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Oncomagnetic patent Fig 2
Bcl-2↓,
BAX↑,
Bak↑,
Cyt‑c↑,
Casp3↑, caspase staining rises progressively until after 30 min most of the cells fluoresce positive for caspase, revealing activation of this enzyme
Casp9↑,
DNAdam↑,
ROS↑, applying the oscillating magnetic field to the tissue increases the production of reactive oxygen species (ROS )
lactateProd↑,
Apoptosis↑,
MPT↑, opening of the mitochondrial membrane permeability transition pore
*selectivity↑, repetitive magnetic stimulation has shown decreased apoptosis in non -cancerous cells .
eff↑, oncomagnetic therapy may be performed in conjunction with other forms of therapy such as with chemotherapy, other forms of radiative therapy, with drugs and prescriptions, etc
MMP↓, OMF which in turn produces rapidly fluctuating or sustained depolarizations of the mitochondrial membrane potential (MMP) in the tissue .
selectivity↑, Because normal cells have a larger amount of mitochondria, have lower demand for ATP, and are not under stress, disruption of electron flow and small amount of ROS formation and MMP depolarization does not trigger apoptosis
TCA?, decrease in Krebs cycle metabolites
H2O2↑, increase in peroxide levels in GBM cells following stimulation by the system 100 using a rotating magnet
eff↑, combine the administration of BHB , or acetoacetate , or free fatty acid, or branched chain amino acid, or cryptochrome agonist , or MGMT inhibitor, or DNA alkylating agent, or DNA methylating agent, and OMF as a more effective treatment of cancer
*antiOx↑, upregulation of antioxidant mechanisms due to the application of OMFs further protects non -cancerous cells from any ROS -mediated apoptosis
H2O2↑, The experiments showed rapid increases in the levels of superoxide and H2O2 in GBM cells
eff↓, To test whether cell death is caused by the OMF - induced increase in ROS , a potent antioxidant Trolox was used to counteract it, while measuring the decrease in GBM cell count due to 4 h exposure to OMF.
GSH/GSSG↓, GSH/GSSG ratio almost exactly half that seen in control cells
*toxicity∅, No Cytotoxic Effect in Normal Cells
OS↑, OMF -Induced Prolongation of Survival in a Mouse Xenograft Model of GBM

185- MFrot,  MF,    Case Report: End-Stage Recurrent Glioblastoma Treated With a New Noninvasive Non-Contact Oncomagnetic Device
- Human, GBM, NA
TumVol↓, OMF for 5 weeks was well tolerated, with 31% reduction of contrast-enhanced tumor volume
Dose↝, we estimated that the combined effective field (at least 1 mT in strength) of the 3 oncoscillators covered the entire brain. 2 and 3 2-hour sessions, respectively, with 1-hour breaks between the sessions.
cognitive↑, The patient’s caregivers reported subjective improvement in speech and cognitive function.

203- MFrot,  MF,    Rotating Magnetic Field Induced Oscillation of Magnetic Particles for in vivo Mechanical Destruction of Malignant Glioma
- vitro+vivo, GBM, U87MG
lysoMP↓, tear the lysosomal membrane
TumVol↓, 1hr, 40% distroyed
eff↑, MPs can be internalized into the glioma cells and induce apoptosis under a rotating magnetic field
Apoptosis↑, Intratumoral MPs induces apoptosis
Ca+2↑, induce chemical ionic signal such as calcium to nitiate programmed cell death upon exposure to an alternating field [9].

204- MFrot,  MF,    Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization
- in-vivo, AD, NA
*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice

205- MFrot,  MF,    Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer Metastasis
- vitro+vivo, BC, MDA-MB-231
OS↑, 31-46% prolonged survival
F-actin↓, decrease F-actin formation in vitro and in vivo
TumCI↓,
TumCMig↓, >4.5hrs
Rho↓,
selectivity↑, F-actin in noncancerous breast cells is much less sensitive than that in breast cancer cells, which indicate that the normal cells in our human bodies are less likely to be agitated by these magnetic fields.

209- MFrot,  MF,    The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study
- Human, NA, NA
*SOD↑, RFM can reduce oxidative stress, as evidenced by higher SOD and CAT activities in the CG than in samples placed in the RFM.
*Catalase↑,
*ROMO1↑, required 3hrs
*MDA↓, Too long a stay in the RMF at the frequency of 50 Hz increased the level
*TAC↑, RFM at 50 Hz increased the TAC level,
*ROS↓, In the case of ROMO1, it is stated that 1 h 25 Hz are the optimal conditions for no increased production of ROS.

212- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease mice
- in-vivo, AD, SH-SY5Y
*β-Amyloid↓, Aβ amyloid fibril formation
*cognitive↑,
*motorD↑, RMF improves motor and exploration abilities in APP/PS1 mice
*ROS↓, RMF reduces oxidative stress in APP/PS1 mouse brains and lipid deposition in the liver
*memory↑, RMF significantly alleviates spatial memory impairments in APP/PS1 mice
*Aβ?, 0.4 T RMF inhibits Aβ amyloid fibril formation in vitro

213- MFrot,  MF,    Rotating Magnetic Field-Assisted Reactor Enhances Mechanisms of Phage Adsorption on Bacterial Cell Surface
- in-vitro, NA, NA
CellMemb↑, more negatively charged outer membrane. Improves adsorption thru cell membrane.

200- MFrot,  MF,    Moderate intensity low frequency rotating magnetic field inhibits breast cancer growth in mice
- in-vivo, BC, MDA-MB-231 - in-vivo, BC, MCF-7
ALAT↓,
TumVol↓, reduced tumor size in LF-RMF group. In the end of the experiment on day 11, the tumor was removed and weighted, which showed a 35% reduction in tumor weigh

199- MFrot,  MF,    Modulation of Cellular Response to Different Parameters of the Rotating Magnetic Field (RMF)—An In Vitro Wound Healing Study
- in-vivo, Wounds, L929 - NA, NA, HaCaT
*ROS↑,
*Ca+2↓,
*other↝, (i) WMF can evoke new tissue production/regeneration (stem cell proliferation and subsequent differentiation) due to manipulation of ROS levels and also downstream heat shock protein 70 (Hsp70) expression
*other↝, (ii) The magnetic field causes changes in membrane potential and temporary membrane permeabilization that affects sodium content and potassium-efflux or the transmembrane voltage
*other↝, (iii) The calcium gradient between the extracellular and intracellular fluid is a transduction second messenger [28], and its gradient could potentially be affected by EMFs and MFs.
*other↝, (iv) MF may induce changes in enzymatic activities (e.g., enzymes involved in mitochondrial metabolism).
*other↝, (v) MF may cause cytoskeletal organization (due to reorganization of the electrostatically negative charged actin filaments), and those changes may affect the cellular shape, endoplasmic reticulum, mitotic apparatus
*other?, vi) Finally, the RMF creates the mixing process at the micro-level and may affect the energy level; some of the selected molecules strongly influence the transfer processes between the living cells and the culture medium

198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,

195- MFrot,  MF,    Application of Rotating Magnetic Fields Increase the Activity of Antimicrobials Against Wound Biofilm Pathogens
- Human, Wounds, NA

193- MFrot,  MF,    Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions
- in-vivo, Arthritis, NA
BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,

516- MFrot,  immuno,  MF,    Anti-tumor effect of innovative tumor treatment device OM-100 through enhancing anti-PD-1 immunotherapy in glioblastoma growth
- vitro+vivo, GBM, U87MG
TumCP↓,
Apoptosis↑,
TumCMig↓,
ROS↑, treatment with OM-100 led to an increase in intracellular ROS levels
PD-L1↑, upregulating PD-L1 expression, thereby enhancing the efficacy of anti-PD-1 immunotherapy
TumVol↓, in mice
eff↑, enhance the efficacy of anti‑PD‑1 immunotherapy in vivo
*toxicity∅, OM-100 did not result in noteworthy changes in the blood routine parameters (Gran, HCT, HGB, Lymph, MCH, MCV, PLT, RBC, MPV, and WBC) and biochemical indicators (ALT, AST, T-BIL, CREA, TG, TC, HDL-c, and LDL-c) in normal mice
eff↑, Particularly, there was a more pronounced response to anti-PD-1 therapy in patients whose tumors expressed PD-L1 3
*toxicity∅, OM-100 treatment in healthy mice showed no adverse effects, indicating its safety for normal tissues.
Dose↝, 24-day treatment with a magnetic field intensity of 1.066 mT and a frequency of 100 kHz (figure shows motor driven 120Hz, 7200rpm pulsed
tumCV↓, anti-tumor efficacy of OM-100 treatment, which by impairing cell viability, increasing apoptosis, inhibiting cell migration, and invasion capabilities, as well as promoting oxidative stress.
TumCI↓,

191- MFrot,  MF,    Early exposure of rotating magnetic fields promotes central nervous regeneration in planarian Girardia sinensis
- in-vivo, Nor, NA
*EGR4↑,
*Netrins↑, Netrin 2
*NSE↑,
*NPY↑,

186- MFrot,  MF,    Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields
- in-vitro, GBM, GBM - in-vitro, Lung, NA
mt-ROS↑,
Casp3↑,
selectivity↑, OMF induces highly selective cell death of patient derived GBM cells associated with activation of caspase 3, while leaving normal tissue cells undamaged
TumCD↑,
ETC↓, The underlying mechanism is a marked increase in ROS in the mitochondria, possibly in part through perturbation of the electron flow in the respiratory chain.

190- MFrot,  MF,    The efficacy and safety of low-frequency rotating static magnetic field therapy combined with chemotherapy on advanced lung cancer patients: a randomized, double-blinded, controlled clinical trial
- Human, Lung, NA
*IP-10/CXCL-10↑, MF group patients had higher concentrations of IP-10 and GM-CSF, and lower concentration of sTREM-1 in plasma
*GM-CSF↑, in PLASMA
*TREM-1↓, sTREM-1, in PLASMA

187- MFrot,  MF,    Method for noninvasive whole-body stimulation with spinning oscillating magnetic fields and its safety in mice
- in-vivo, GBM, NA
selectivity↑, Our in vitro experiments demonstrated selective cancer cell death while sparing normal cells by sOMF-induced increase in intracellular reactive oxygen species (ROS) levels due to magnetic perturbation of mitochondrial electron transport.
ROS↑,
*ROS∅,
*toxicity∅, no significant adverse effects of chronic or acute sOMF stimulation on the health, behavior, electrocardiographic and electroencephalographic activities, hematologic profile, and brain and other tissue and organ morphology of treated mice

189- MFrot,  MF,    Cancer treatment by magneto-mechanical effect of particles, a review
- vitro+vivo, Var, NA
CellMemb↑, damage the cell membrane
lysoMP↑, through heat and/or mechanical damage
ERK↑,
Apoptosis↑,

188- MFrot,  MF,    Spinning magnetic field patterns that cause oncolysis by oxidative stress in glioma cells
- in-vitro, GBM, GBM115 - in-vitro, GBM, DIPG
ROS↑, both GBM and DIPG cells ROS generated by sOMF
SDH↓, Complex II succinate dehydrogenase
eff↓, antioxidant Trolox reverses the cytotoxic effect of sOMF on glioma cells indicating that ROS play a causal role in producing the effect
RPM↑, we hypothesized that the interaction of weak and intermediate strength magnetic fields with the RPM mechanism in the mitochondrial ETC can perturb the electron transfer process (MEP hypothesis) to generate superoxide.
eff↓, We observed that Helmholtz coil did not produce any significant increase in ROS at 2 and 4 h during stimulation or 2 h poststimulation in GBM and DIPG cells
eff↑, oscillating field alone is not sufficient to induce ROS and that the changing angle of the magnetic field axis is also required to achieve this effect.
eff↝, repeated pulse trains rising to and declining from the peak frequency with intervening pauses are sufficient to achieve near maximum level of increase in ROS
eff↝, One spinning magnet or three spinning magnets generate similar cellular ROS levels and the effect of variation of the stimulus off period.
Casp3↑, caspase 3 activation
eff↝, This indicates that the total amount of energy delivered to cancer cells is clearly not the determinant of the potency of stimulation. Instead, it appears that the longer Toff between stimuli of 750 ms in the 4-h stimulation, as opposed to 250 ms in
SOD↓, critical rise in superoxide in two types of human glioma cells (implies SOD capacity exceeded)
ETC↓, found support for the hypothesis that the sOMF-induced increase in ROS is likely due to perturbation of the electron transfer process in the mitochondrial electron transport chain (ETC)

228- MFrot,  MF,    Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
- NA, MS, NA
*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α↓,
*Treg lymp↓, increasing the proportion of Treg cells
*IFN-γ↓, However, on day 20 after immunization, IFN-γ and IL-17A levels in the serum of EAE mice were significantly reduced by the exposure of RMF
*IL17↓,
*CXCc↓, mRNA expression of IFN chemokines (CXCL-1 and CXCL-2), and IL-17 chemokines (CXCL-9 and CXCL-10) had also significantly reduced in EAE mice after RMF exposure.

184- MFrot,  MF,    Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells
- in-vitro, GBM, GBM
ROS↑, sOMF
mitResp↓, Inhibit Mitochondrial Respiration
mtDam↑, Produce Loss of Mitochondrial Integrity
Dose↝, Repeated intermittent sOMF was applied for 2 hours at a specific frequency, in the 200-300 Hz frequency range, with on-off epochs of 250 or 500 ms duration.
MMP?, ROS generation has been shown to be driven, in part, by elevated mitochondrial membrane chemiosmotic potential (ΔΨ) and ubiquinol (QH2)
OCR↓, Immediately after cessation of field rotation we observe a loss of mitochondrial integrity (labeled LMI), with a very rapid increase in O2 consumption
mt-H2O2↑, We have previously demonstrated that sOMF treatment of cells generates superoxide/hydrogen peroxide in the mitochondrial matrix
eff↓, we repeated the same experiment in the presence of Trolox, which protects thiols from ROS oxidation (47). sOMF treatment of RLM in State 3u pre-treated with Trolox (15 μM), show minimal inhibition,
SDH↓, SDH Inhibition by sOMF in State 3u RLM Is Caused by ROS Generation
Thiols↓, suggest that thiol oxidation in SDH may result from sOMF.
GSH↓, Glutathione in the mitochondrial matrix can provide some protection from ROS, but after solubilizing the mitochondria, this protection is lost and the SDH becomes more sensitive to sOMF.
TumCD↑, sOMF is highly effective at killing non-dividing GBM cell cultures,
Casp3↑, caspase-3 activation 1 h after sOMF
Casp7↑, rapid activation of caspase-3/7
MPT↑, OMF-treated cell that causes near simultaneous MPT, release of cytochrome c and other apoptosis-inducing factors, resulting in caspase-3/7 activation in these GBM cells.
Cyt‑c↑,
selectivity↑, differential sensitivity to sOMF of cancer cells over ‘normal’ cells becomes apparent. rapid increase in the reactive oxygen species (ROS) in the mitochondria to cytotoxic levels only in cancer cells, and not in normal human cortical neurons
GSH/GSSG↓, increasing GSSG/GSH ratio
ETC↓, completely arrest electron transport in isolated, respiring, rat liver mitochondria and patient derived glioblastoma (GBM)

595- MFrot,  VitC,  MF,    The Effect of Alternating Magnetic Field Exposure and Vitamin C on Cancer Cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, CRC, SW-620 - in-vitro, NA, HT1080 - in-vitro, Pca, PC3 - in-vitro, OS, U2OS - in-vitro, BC, MCF-7 - in-vitro, Nor, CCD-18Co
TumCD↑, An 80 percent cell death (20 percent survival) was achieved with 160 mg/dL of vitamin C in the magnetic field treatment group. It required 360 mg/dL to achieve the same effect with vitamin C only treatment group.
eff↑, vitamin C combined with low frequency magnetic field or rotating magnetic field reduces the amount of vitamin C to induce 50 percent inhibition of tumor cells.
*TumCG∅, For normal cell line of colon fibroblast magnetic field did not potentiate inhibition of cell growth. These are all mono-layer cell culture.

1737- MFrot,  Fe,  MF,    Feature Matching of Microsecond-Pulsed Magnetic Fields Combined with Fe3O4 Particles for Killing A375 Melanoma Cells
- in-vitro, MB, A375
Dose∅, current amplitude of 1640 A, a pulse width of 28 μs and a frequency of 1 Hz nanorods, with a length of about 100 nm and a diameter of about 20 nm strongest magnetic flux density at the center of the coil reaching 1.96 T.
tumCV↓, killing rate of μs-PMF with nanorods was 39.6% higher than that of μs-PMF alone

230- MFrot,  MF,    Study on the Effect of Rotating Magnetic Field on Cellular Response of Mammalian Cells
- in-vitro, Nor, L929
*ALDH↑, cell cultures treated with the highest magnetic induction (10.06 mT, 50 Hz) showed higher dehydrogenases activity than the cells exposed to the lower magnetic flux density (1.23 mT–6.58 mT

229- MFrot,  MF,    Molecular mechanism of effect of rotating constant magnetic field on organisms
- in-vivo, Nor, NA
*NO↑, lasted 3hrs
*5HT↓, 5-HT content in mice brain decreased significantly after the treatment of RCMF
*eff↝, 5-HT content reached the lowest point after magnetic field treatment for 90 min and 60 min in decortex brain and small intestine respectively, but it returned to the normal level after two hours
*eff↝, inhibition of magnetic field on vomiting reaction was parallel to the decreasing level of 5-HT content in brain and small intestine tissue
*β-Endo↑, After animals and voluntary patients were treated by magnetic field, their plasma β-endorphin increased 23 times higher than before.
*other↓, Under the action of magnetic field, the synthesis and secretion of melatonin are weakened in pineal gland, and the melatonin content decreases in plasma

214- MFrot,  MF,    Modification of bacterial cellulose through exposure to the rotating magnetic field
- in-vitro, Nor, NA
CellMemb↑, higher water absorption
GlucoseCon↓, The bacteria exposed to the RMF used 9% less glucose as compared with the microorganisms from the control culture

227- MFrot,  MF,    Low Frequency Magnetic Fields Induce Autophagy-associated Cell Death in Lung Cancer through miR-486-mediated Inhibition of Akt/mTOR Signaling Pathway
- in-vivo, Lung, A549 - in-vitro, Lung, A549
TumCG↓,
miR-486↑, decreased expression of miR-486 and an increased expression of BCAP were found in tumor tissues of lung cancer patients
BCAP↓,
Apoptosis↑,
ROS↑,
TumAuto↑, miR-486 is required for LF-MFs triggered autophagy
LC3II↑,
ATG5↑,
Beclin-1↑,
p62↑, blocked p62 degradation
TumCP↓,

226- MFrot,  MF,    Involvement of midkine expression in the inhibitory effects of low-frequency magnetic fields on cancer cells
- in-vitro, NA, A549 - in-vitro, NA, LoVo
TumCP↓, inhibit tumor cell proliferation
eff↝, We found that the inhibitory effect of MFs on BGC-823 cell growth was enhanced by increasing the magnetic flux density from 0.05 to 0.4 T(Fig. 2A) and increasing the frequency from 0 to 7.5 Hz.

225- MFrot,  MF,    Extremely low frequency magnetic fields regulate differentiation of regulatory T cells: Potential role for ROS-mediated inhibition on AKT
- vitro+vivo, Lung, NA
MMP2↓,
MMP9↓,
FOXP3↓,
ROS↑,
p‑Akt↓,

217- MFrot,  MF,    Effect of low-frequency rotary magnetic fields on advanced gastric cancer
- in-vivo, GC, HL-60 - in-vivo, GC, SK-HEP-1
OS↑, 8months compared to 3-5 normally
Pain↓, low-frequency rotary MFs improved abdominal pain in 9/21 (42.9%), nausea/vomiting in 4/21 (19.0%), weight loss in 11/21 (52.4%), ongoing blood loss in 2/21 (9.5%), physical strength in 5/21 (23.8%), and sleep quality in 4/21 (19.0%) patients.
ChemoSideEff↓,
Weight↑,
Strength↑,
Sleep↑,

215- MFrot,  MF,    Magneto-mechanical destruction of cancer-associated fibroblasts using ultra-small iron oxide nanoparticles and low frequency rotating magnetic fields
- in-vitro, PC, CAF
TumVol↓, 34% ratio in cell death induction
lysoMP↑, induce lysosome membrane permeabilization RMF exposure caused lysosome rupture
CAFs/TAFs↓,
eff↑, disrupt the tumor microenvironment through mechanical forces generated by mechanical activation of magnetic nanoparticles upon low-frequency rotating magnetic field exposure

216- MFrot,  MF,    Elongated Nanoparticle Aggregates in Cancer Cells for Mechanical Destruction with Low Frequency Rotating Magnetic Field
- in-vitro, GBM, U87MG
lysoMP↓, damage
CellMemb↑, Physical destruction of cell membrane

224- MFrot,  MF,    A pilot study of extremely low-frequency magnetic fields in advanced non-small cell lung cancer: Effects on survival and palliation of general symptoms
- Human, NSCLC, NA
PleEff↓,
breath↑, decreased shortness of breath
Pain↓,
Appetite↑,
Strength↑,
BowelM↑, regular Bowel Movements
OS↑, ELF-MFs may prolong survival and improve general symptoms of advanced NSCLC patients. Median survival 6 mnts vs 4mnts. median survival of patients treated with ELF-MFs was longer than that of those receiving supportive care.

218- MFrot,  MF,    Extremely low frequency magnetic fields inhibit adipogenesis of human mesenchymal stem cells
- in-vitro, Nor, NA
*PPARγ↓, PPARg2
*p‑JNK↑, p-JNK
*Wnt↑,
*ALP∅, ELF-MF had no effects on the expression of ALP, COL1a1, Runx2, and OCN
*COL1∅,
*RUNX2∅,
*OCN∅,
*FABP4↓, ELF-MF exposure for 15 days resulted in a decrease in PPARg2 and FABP4
*p‑JNK↑, p-JNK was increased after ELF-MF exposure
*Diff↓, adipogenic differentiation of MSCs could be inhibited by ELF-MF of 7.5 Hz, 0.4 T, suggesting the inhibitory effect of ELF-MF on obesity may be attributed to the inhibition of differentiation of MSCs into adipocytes.

219- MFrot,  MF,    The expression and intranuclear distribution of nucleolin in HL-60 and K-562 cells after repeated, short-term exposition to rotating magnetic fields
- in-vitro, AML, HL-60 - in-vitro, AML, K562
nucleolin↑, HL-60 cells showed increase of nucleolin expression in nucle

220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)

221- MFrot,  MF,    Low Frequency Magnetic Fields Enhance Antitumor Immune Response against Mouse H22 Hepatocellular Carcinoma
- in-vivo, Liver, NA
OS↑,
TumCG↓, inhibit
IL6↓,
GM-CSF↓,
CXCc↓, keratinocyte-derived chemokine (KC)
Macrophages↑,
DCells↑,
CD4+↑,
CD8+↑,
IL12↑,

222- MFrot,  MF,    LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway
- in-vitro, Lung, A549
TumCG↓,
OS↑,
miR-34a↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

223- MFrot,  MF,    The effect of rotating magnetic fields on the growth of Deal's guinea pig sarcoma transplanted subcutaneously in guinea pigs
- in-vivo, NA, NA
TumCG↓,

656- MNPs,  MF,    Effects of combined delivery of extremely low frequency electromagnetic field and magnetic Fe3O4 nanoparticles on hepatic cell lines
- in-vitro, HCC, HepG2 - in-vitro, Nor, HL7702
BioAv↑, higher MNP uptake ratio
Apoptosis↑,
*toxicity↓, ELFF and MNPs produced greater apoptosis of hepatoma cell lines than of healthy control hepatic cells.

356- SNP,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF-7 - in-vitro, Bladder, HTB-22
Apoptosis↑,
P53↑, Up-regulation in the expression level of p53, iNOS and NF-kB genes as well as down-regulation of Bcl-2 and miRNA-125b genes were detected post treatment.
iNOS↑,
NF-kB↑,
Bcl-2↓,
ROS↑, the present study evaluated the levels of ROS as well as the antioxidant enzymes (SOD and CAT)
SOD↑,
TumCCA↑, S phase arrest and accumulation of cells in G2/M phase was observed following exposure to AgNPs and EMF, respectively.
eff↑, Apoptosis induction was obvious following exposure to either ELF-EMF or AgNPs, however their apoptotic potential was intensified when applied in combination
Catalase↑, Catalase (CAT)
other↑, swollen cells, swollen nuclei with mixed euchromatin and heterochromatin, ruptured cell membranes

400- SNP,  MF,    Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field
- in-vitro, Laryn, HEp2
TumCP↓, especially in the G0/G1 and S phases.
Casp3↑,
P53↑,
Beclin-1↑,
TumAuto↑,
GSR↑, oxidative stress biomarker
ROS↑, oxidative stress biomarker
MDA↑, oxidative stress biomarker
ROS↑,
SIRT1↑,
Ca+2↑, induce apoptosis in osteoclasts by increasing intracellular and nucleus Ca2+ concentration
Endon↑, increases endonuclease activity
DNAdam↑,
Apoptosis↑,
NF-kB↓,

402- SNP,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF-7
P53↑,
iNOS↑,
NF-kB↑,
Bcl-2↓,
miR-125b↓,
ROS↑, 2.9x for 2hr
SOD↑, 2.4x for 2hr

593- VitC,  MF,    Protective Effect of Ascorbic Acid on Molecular Behavior Changes of Hemoglobin Induced by Magnetic Field Induced by Magnetic Field
RPM↓, Ascorbic acid adds protective effect from magnetic fields

588- VitC,  MF,    Preparation of magnetic nanoparticle integrated nanostructured lipid carriers for controlled delivery of ascorbyl palmitate
other↑, AA, as an antitumor agent

580- VitC,  MF,    Extremely low frequency magnetic field induces oxidative stress in mouse cerebellum
- in-vivo, Nor, NA
*other↓, ascorbic acid levels were significantly decreased by ELF-MF exposure
*MDA↓, significant increase in malondialdehyde level
*GPx∅, increase in superoxide dismutase without alteration in glutathione peroxidase activity
*SOD↑, SOD activity was significantly increased in mouse cerebellum
*GSH∅, GSH contents were not significantly different from sham controls,

579- VitC,  MF,    Effect of Magnetic Field on Ascorbic Acid Oxidase Activity, I
- in-vitro, NA, NA
other↝, significant influence on the activity of the enzyme ascorbic acid oxidase


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 253

Results for Effect on Cancer/Diseased Cells:
ACAA1↓,1,   ADP:ATP↓,2,   Akt↓,3,   p‑Akt↓,3,   ALAT↓,1,   angioG↓,7,   angioG↑,1,   AntiCan↑,2,   AntiTum↑,1,   Apoptosis↑,35,   Appetite↑,2,   ATF3↑,1,   ATG5↑,1,   ATM↑,1,   ATP↓,1,   ATP↑,2,   ATP⇅,1,   ATP∅,1,   p‑BAD↓,1,   Bak↑,1,   BAX↑,5,   BCAP↓,1,   Bcl-2↓,5,   Beclin-1↑,2,   BioAv↑,1,   BMD↑,1,   BMPs↑,1,   BowelM↑,2,   breath↑,2,   Ca+2↓,1,   Ca+2↑,26,   Ca+2↝,2,   i-Ca+2↑,1,   CAFs/TAFs↓,1,   Calcium↑,1,   cAMP⇅,1,   Cartilage↑,1,   Casp↑,1,   Casp↝,1,   Casp3↓,1,   Casp3↑,8,   cl‑Casp3↑,1,   Casp7↓,1,   Casp7↑,4,   cl‑Casp7↑,1,   cl‑Casp8↑,1,   Casp9↑,3,   cl‑Casp9↑,1,   Catalase↓,1,   Catalase↑,3,   CCDC150↓,1,   CD133↓,1,   CD4+↓,1,   CD4+↑,1,   CD44↓,1,   CD8+↓,1,   CD8+↑,1,   p‑CDK2↓,1,   CellMemb↑,7,   chemoP↑,1,   ChemoSen↑,10,   ChemoSen∅,1,   ChemoSideEff↓,1,   p‑CHK1↓,1,   Chk2↑,2,   CHOP↑,1,   cMyc↓,1,   cognitive↑,2,   COL4↓,1,   COX2↓,1,   CSCs↓,2,   CXCc↓,1,   CycB↓,1,   cycE↓,1,   Cyt‑c↑,4,   Cyt‑c↝,1,   DCells↑,2,   DHCR24↑,1,   Diff↑,1,   DNAdam↑,12,   Dose?,1,   Dose↓,1,   Dose↝,4,   Dose∅,2,   E2Fs↓,1,   ECAR↓,1,   ECM/TCF↓,1,   eff↓,11,   eff↑,30,   eff⇅,1,   eff↝,13,   EGFR↓,1,   EGFR↝,1,   p‑EGFR↓,1,   Endon↑,1,   EPR↑,2,   ER Stress↓,1,   ER Stress↑,3,   ERK↑,1,   p‑ERK↑,2,   p‑ERK↝,1,   ETC↓,3,   F-actin↓,1,   FABP4↓,1,   Fas↑,1,   Fenton↑,1,   Ferritin↓,1,   Ferroptosis↑,1,   FOSB↑,1,   FOXP3↓,1,   GlucoseCon↓,1,   Glycolysis↓,2,   Glycolysis∅,1,   GM-CSF↓,1,   GPx↓,1,   GPx1↓,1,   GPx1↑,1,   GPx4↓,1,   GRP78/BiP↑,2,   GRP94↑,1,   GSH↓,1,   GSH/GSSG↓,2,   GSK‐3β↑,1,   GSR↑,1,   H2O2↑,4,   mt-H2O2↑,1,   Hif1a↓,1,   HSP70/HSPA5↓,2,   HSP70/HSPA5↑,7,   HSP70/HSPA5∅,1,   HSP90↓,2,   HSPs↑,1,   HSPs∅,1,   IFN-γ↓,1,   IL1↑,1,   IL10↑,2,   IL12↑,1,   IL17↓,2,   IL22↓,1,   IL23↓,1,   IL28↓,1,   IL6↓,1,   IL6↑,1,   IL9↓,1,   iNOS↑,2,   Iron↑,1,   ITGA1∅,1,   ITGA11↓,1,   ITGA5∅,1,   ITGB1∅,1,   ITGB3∅,1,   ITGB4∅,1,   JNK↑,1,   lactateProd↑,1,   LAMB3↑,1,   LC3II↑,1,   LIF↑,1,   lysoMP↓,2,   lysoMP↑,2,   Macrophages↑,1,   MAPK↓,1,   MAPK↑,3,   Mcl-1↓,1,   MDA↑,2,   miR-125b↓,1,   miR-126↓,1,   miR-129-5p↑,1,   miR-155↑,1,   miR-200c↓,1,   miR-21↑,1,   miR-210↑,1,   miR-34a↑,1,   miR-486↑,1,   mitResp↓,1,   mitResp↑,1,   MMP?,1,   MMP↓,6,   MMP↑,1,   MMP1↑,1,   MMP2↓,1,   MMP2↑,2,   MMP2∅,1,   MMP3↑,1,   MMP9↓,1,   MMP9↑,1,   MMP9∅,1,   MMPs↓,1,   MPT↑,2,   mtDam↑,1,   mTOR↓,1,   Nanog↓,1,   Necroptosis↑,1,   necrosis↑,1,   NF-kB↓,1,   NF-kB↑,2,   NO↑,1,   nucleolin↑,1,   OCR↓,1,   OCR↑,1,   OS↑,13,   other↓,3,   other↑,5,   other↝,2,   other∅,1,   OXPHOS↑,3,   P-gp↓,1,   P21↑,2,   p38↑,3,   P53↑,6,   P53↝,1,   p62↑,1,   Pain↓,4,   cl‑PARP↑,3,   PCK1↓,1,   PD-L1↑,1,   PGC-1α↑,1,   i-pH↑,1,   PI3K↓,2,   PKM2↓,1,   PleEff↓,1,   PLIN1↓,1,   PPARγ↑,1,   Prx6↑,1,   PTEN↓,1,   Pyruv↓,2,   QoL↑,1,   radioP↑,1,   RadioS↑,4,   RANTES↓,1,   RAS↑,1,   Rho↓,1,   ROS↑,47,   ROS↝,2,   mt-ROS↑,2,   RPM↓,1,   RPM↑,7,   SDH↓,2,   selectivity↑,22,   SIRT1↑,1,   SIRT3↑,1,   Sleep↑,1,   Slug↓,1,   p‑SMAD2↓,1,   SMAD3↓,1,   p‑SMAD3↓,1,   SOD↓,3,   SOD↑,2,   SOD1↓,1,   SOD1↑,1,   SOD2↓,1,   SOD2↑,2,   SOX2↓,1,   STAT3↑,1,   p‑STAT3↑,1,   Strength↑,3,   survivin↓,2,   T-Cell↑,1,   TCA?,1,   TfR1/CD71↓,1,   TGF-β↓,2,   THBS2↓,1,   Thiols↓,1,   TNF-α↓,2,   TNF-α↑,1,   TRAIL↓,1,   TRPC1↑,1,   TRPV1↑,1,   TumAuto↑,6,   TumCCA↑,11,   TumCD↑,10,   TumCD∅,1,   TumCG↓,20,   TumCI↓,6,   TumCMig↓,7,   TumCP↓,15,   TumCP∅,1,   tumCV↓,6,   TumMeta↓,4,   TumVol↓,13,   Twist↓,1,   UCP1↓,1,   UPR↑,2,   VEGF↓,1,   VEGF↑,1,   VEGFR2↓,2,   VGCC↑,1,   Vim↓,1,   Warburg↓,1,   Weight↑,1,   β-catenin/ZEB1↓,2,   γH2AX↑,1,   p‑γH2AX↑,1,  
Total Targets: 292

Results for Effect on Normal Cells:
5HT↓,1,   5HT↑,2,   Ach↑,1,   AChE↓,1,   ADP:ATP↓,1,   Akt↓,2,   Akt↑,2,   p‑Akt↓,1,   p‑Akt↑,1,   ALDH↑,1,   ALP↑,2,   ALP∅,1,   AMPK↑,1,   angioG↑,7,   angioG↝,1,   AntiAge↑,1,   antiOx↑,9,   Apoptosis↓,6,   APP∅,1,   ARG↑,1,   ATP↑,3,   Aβ?,1,   Aβ↓,9,   Aβ∅,2,   BACE↓,1,   BAD↓,1,   BAX↓,3,   BBB↑,1,   Bcl-2↑,1,   Bcl-2∅,1,   Bcl-xL↑,1,   BDNF↑,10,   BioAv↓,1,   BioAv↑,1,   BioEnh↑,4,   BMD↑,11,   BMP2↑,2,   BMPs↓,1,   BMPs↑,1,   Ca+2↓,5,   Ca+2↑,11,   Ca+2∅,1,   i-Ca+2↓,1,   cAMP↑,2,   cardioP↑,3,   Cartilage↑,2,   Casp1↓,1,   cl‑Casp1↓,1,   proCasp1↓,1,   Casp3↓,2,   Catalase↑,8,   CD4+↑,1,   CDK5↓,1,   cFos↑,1,   cognitive↑,19,   cognitive∅,1,   COL1∅,1,   COL2A1↑,2,   COX2↓,2,   p‑CREB↑,1,   CXCc↓,1,   Cyt‑c↑,2,   cytoP↑,1,   Diff↓,1,   Diff↑,9,   Dose↝,18,   Dose∅,1,   E2Fs↑,1,   ECAR↓,1,   ECAR↑,1,   eff↓,6,   eff↑,16,   eff↝,5,   EGR4↑,1,   ER Stress↑,1,   ERK↓,1,   ERK↑,2,   p‑ERK↓,1,   p‑ERK↑,2,   ETC↓,1,   F-actin↑,1,   FABP4↓,1,   FAK↑,2,   FAO↓,1,   FAO↑,1,   FGF↑,5,   GLUT1↑,2,   GLUT4↑,1,   Glycolysis↓,1,   Glycolysis↑,2,   GM-CSF↑,1,   GPx↑,4,   GPx∅,1,   GPx1↑,5,   GPx3↑,1,   GPx4↑,5,   GSDMD?,1,   GSDMD↓,1,   GSH↑,1,   GSH∅,1,   GSK‐3β↓,1,   p‑GSK‐3β↑,1,   GSR↑,3,   GSSG↓,1,   GutMicro↑,1,   hepatoP↑,1,   HEY1↑,1,   HGF/c-Met↑,1,   HIF-1↓,1,   Hif1a↑,2,   Hif1a↝,1,   Hif1a∅,2,   HIF2a↑,1,   HK2↑,2,   HO-1↑,1,   HSP70/HSPA5↑,5,   HSPs↑,1,   IFN-γ↓,1,   IGF-1↑,1,   p‑IKKα↓,2,   IL1↓,2,   IL1↑,1,   IL10↑,5,   IL17↓,1,   IL1β↓,6,   IL1β↑,1,   IL2↑,1,   IL4↑,1,   IL6↓,6,   IL6↑,1,   IL8↓,2,   Inflam↓,26,   Inflam∅,1,   iNOS↓,3,   iNOS↑,1,   Insulin↓,1,   IP-10/CXCL-10↑,1,   ITGB1↑,1,   p‑IκB↓,1,   p‑JNK↓,1,   p‑JNK↑,3,   Keap1↓,1,   lactateProd↓,1,   LDH↓,1,   LDHB↑,1,   MAPK↓,1,   MAPK↑,2,   MCP1↓,1,   MCP1↑,2,   MDA↓,5,   MDA↑,1,   memory↑,19,   memory∅,2,   MIP‑1α↓,1,   miR-34b-5p↓,1,   mitResp↓,1,   MMP↑,3,   MMP⇅,1,   MMP↝,1,   MMP∅,1,   MMP-10↓,1,   MMP1↓,1,   MMP2↑,2,   MMP9↓,3,   MMP9↑,2,   MMPs↑,1,   Mood⇅,1,   motorD↑,10,   mPGES-1↓,1,   MPT↑,1,   MSCs↑,1,   mTOR↓,3,   mTOR↑,2,   mTOR↝,1,   MyD88↓,1,   NAD↑,1,   necrosis↓,1,   Netrins↑,1,   neuroP↑,18,   NF-kB↓,6,   NGF↑,1,   NLRP3↓,2,   NO↓,4,   NO↑,5,   NOTCH↑,1,   NOTCH1↑,1,   NPY↑,1,   NRF2↑,3,   NSE↑,1,   OCN↑,1,   OCN∅,1,   OCR↑,1,   mt-OCR↑,1,   OPN↑,1,   OS↑,1,   other?,2,   other↓,2,   other↑,11,   other↝,9,   OXPHOS↓,2,   OXPHOS↑,2,   p38↑,2,   p‑p38↓,1,   p‑p65↓,1,   p‑P70S6K↑,1,   Pain↓,5,   PDGF↑,1,   PDGFR-BB↑,1,   PFKL↑,2,   PFKM↑,2,   PFKP↑,1,   PGC-1α↑,2,   PGE2↓,3,   PGE2↑,1,   pH↑,1,   PI3K↓,1,   PI3K↑,1,   PKA↑,1,   PKCδ↓,1,   PKM2↑,2,   PONs↓,1,   PPARγ↓,1,   PPP↓,1,   PSD95↑,1,   PTEN↑,1,   QoL↑,4,   RKIP↑,1,   ROMO1↑,1,   ROS↓,28,   ROS↑,8,   ROS⇅,1,   ROS∅,1,   mt-ROS↑,2,   RUNX2↑,1,   RUNX2∅,1,   selectivity↑,2,   SMAD4↑,1,   SMAD5↑,1,   SOD↑,9,   SOD1↑,5,   SOD2↓,1,   SOD2↑,5,   SOX9↑,2,   SREBP1↓,1,   STAC2↑,1,   STAT3↓,2,   p‑STAT3↓,1,   TAC↑,1,   p‑tau↓,2,   TCA↑,1,   TGF-β↑,4,   TGF-β1↑,1,   TIMP1↑,2,   TIMP2↑,1,   TLR4↓,1,   TNF-α↓,8,   TNF-α↑,1,   toxicity?,1,   toxicity↓,5,   toxicity∅,9,   Treg lymp↓,1,   TREM-1↓,1,   TRPC1↑,1,   Trx↓,1,   TumCG↑,1,   TumCG∅,1,   TumCMig↑,1,   tumCV↑,1,   VEGF↓,1,   VEGF↑,11,   VEGFR2↑,1,   VGCC↑,1,   Weight∅,1,   Wnt↑,3,   YAP/TEAD↑,1,   β-Amyloid↓,1,   β-catenin/ZEB1↑,4,   β-Endo↑,1,  
Total Targets: 278

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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