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↓, PDGF↓, EGFR↓, ITG">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

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

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

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

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

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↓,

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 (

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.

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

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)

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).

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.

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)

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.

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)

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

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

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.

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.

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.

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.

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.

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.

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

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↑,

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

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↓,

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

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↑,

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.

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

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.

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

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↑,

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

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.

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↑,

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↓,

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.

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.

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.

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).

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↑,

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

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↓,

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↑,

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

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?,

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↓,

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↓,

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↑,

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

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.

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↑,

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.

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.

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.

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.

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

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

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↑,

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↑,

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

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

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.

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

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

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↑,

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↑,

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%

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.

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

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

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

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↑,

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↑,

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

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

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↓,

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↓,

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

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.

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

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

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

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

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

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.

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

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

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

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

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

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∅,

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. ****

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

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

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

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

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.

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

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

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.

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

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↓,

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

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: 136

Results for Effect on Cancer/Diseased Cells:
ADP:ATP↓,2,   Akt↓,2,   p‑Akt↓,2,   angioG↓,3,   angioG↑,1,   AntiCan↑,1,   Apoptosis↑,22,   ATM↑,1,   ATP↓,1,   ATP↑,2,   ATP⇅,1,   ATP∅,1,   p‑BAD↓,1,   BAX↑,3,   Bcl-2↓,4,   Beclin-1↑,1,   BioAv↑,1,   BMPs↑,1,   Ca+2↓,1,   Ca+2↑,22,   Ca+2↝,1,   i-Ca+2↑,1,   Calcium↑,1,   cAMP⇅,1,   Casp↑,1,   Casp3↓,1,   Casp3↑,4,   cl‑Casp3↑,1,   Casp7↓,1,   Casp7↑,3,   Casp9↑,1,   Catalase↑,3,   CD133↓,1,   CD44↓,1,   CellMemb↑,3,   chemoP↑,1,   ChemoSen↑,8,   ChemoSen∅,1,   p‑CHK1↓,1,   Chk2↑,2,   CHOP↑,1,   cMyc↓,1,   COX2↓,1,   CSCs↓,2,   CycB↓,1,   Cyt‑c↑,1,   Cyt‑c↝,1,   DHCR24↑,1,   DNAdam↑,8,   Dose?,1,   Dose∅,1,   ECAR↓,1,   eff↓,5,   eff↑,15,   eff⇅,1,   eff↝,9,   EGFR↓,1,   p‑EGFR↓,1,   Endon↑,1,   EPR↑,1,   ER Stress↓,1,   ER Stress↑,3,   p‑ERK↑,2,   p‑ERK↝,1,   Fenton↑,1,   Ferroptosis↑,1,   Glycolysis↓,2,   Glycolysis∅,1,   GPx↓,1,   GPx1↓,1,   GPx1↑,1,   GPx4↓,1,   GRP78/BiP↑,2,   GRP94↑,1,   GSK‐3β↑,1,   GSR↑,1,   H2O2↑,2,   Hif1a↓,1,   HSP70/HSPA5↓,2,   HSP70/HSPA5↑,6,   HSP70/HSPA5∅,1,   HSP90↓,2,   HSPs↑,1,   HSPs∅,1,   IL10↑,1,   IL17↓,1,   IL6↑,1,   IL9↓,1,   iNOS↑,2,   Iron↑,1,   ITGA1∅,1,   ITGA5∅,1,   ITGB1∅,1,   ITGB3∅,1,   ITGB4∅,1,   JNK↑,1,   LIF↑,1,   MAPK↓,1,   MAPK↑,2,   MDA↑,2,   miR-125b↓,1,   miR-126↓,1,   miR-129-5p↑,1,   miR-155↑,1,   miR-200c↓,1,   miR-21↑,1,   miR-210↑,1,   mitResp↑,1,   MMP↓,3,   MMP↑,1,   MMP1↑,1,   MMP2↑,2,   MMP2∅,1,   MMP3↑,1,   MMP9↑,1,   MMP9∅,1,   mTOR↓,1,   Nanog↓,1,   Necroptosis↑,1,   necrosis↑,1,   NF-kB↓,1,   NF-kB↑,2,   NO↑,1,   OCR↑,1,   OS↑,4,   other↓,3,   other↑,5,   other↝,2,   other∅,1,   OXPHOS↑,3,   P21↑,2,   p38↑,3,   P53↑,4,   P53↝,1,   Pain↓,1,   cl‑PARP↑,2,   PGC-1α↑,1,   i-pH↑,1,   PI3K↓,2,   PKM2↓,1,   Prx6↑,1,   Pyruv↓,2,   QoL↑,1,   radioP↑,1,   RadioS↑,4,   RAS↑,1,   ROS↑,35,   mt-ROS↑,1,   RPM↓,1,   RPM↑,6,   selectivity↑,12,   SIRT1↑,1,   SIRT3↑,1,   Slug↓,1,   p‑SMAD2↓,1,   p‑SMAD3↓,1,   SOD↓,2,   SOD↑,2,   SOD1↓,1,   SOD1↑,1,   SOD2↓,1,   SOD2↑,2,   SOX2↓,1,   STAT3↑,1,   p‑STAT3↑,1,   survivin↓,1,   TGF-β↓,1,   TNF-α↓,1,   TNF-α↑,1,   TRAIL↓,1,   TRPV1↑,1,   TumAuto↑,4,   TumCCA↑,7,   TumCD↑,3,   TumCD∅,1,   TumCG↓,11,   TumCI↓,3,   TumCMig↓,4,   TumCP↓,12,   TumCP∅,1,   tumCV↓,2,   TumMeta↓,2,   TumVol↓,5,   Twist↓,1,   UPR↑,2,   VEGF↓,1,   VEGF↑,1,   VEGFR2↓,1,   VGCC↑,1,   Vim↓,1,   Warburg↓,1,   β-catenin/ZEB1↓,2,   p‑γH2AX↑,1,  
Total Targets: 193

Results for Effect on Normal Cells:
ADP:ATP↓,1,   Akt↓,1,   Akt↑,2,   p‑Akt↑,1,   ALP↑,1,   angioG↑,4,   angioG↝,1,   antiOx↑,5,   Apoptosis↓,4,   ATP↑,2,   BAD↓,1,   BAX↓,2,   Bcl-2∅,1,   Bcl-xL↑,1,   BioAv↓,1,   BioAv↑,1,   BioEnh↑,4,   BMD↑,5,   BMP2↑,2,   BMPs↓,1,   Ca+2↓,4,   Ca+2↑,7,   Ca+2∅,1,   i-Ca+2↓,1,   cAMP↑,1,   cardioP↑,1,   Cartilage↑,1,   Casp1↓,1,   cl‑Casp1↓,1,   proCasp1↓,1,   Casp3↓,1,   Catalase↑,2,   COL2A1↑,1,   COX2↓,1,   Cyt‑c↑,2,   cytoP↑,1,   Diff↑,6,   Dose↝,3,   Dose∅,1,   E2Fs↑,1,   ECAR↓,1,   eff↓,4,   eff↑,6,   eff↝,2,   ERK↑,1,   p‑ERK↑,2,   FAK↑,1,   FAO↓,1,   FAO↑,1,   FGF↑,3,   GLUT1↑,2,   GLUT4↑,1,   Glycolysis↓,1,   Glycolysis↑,2,   GPx↑,3,   GPx∅,1,   GPx1↑,3,   GPx4↑,3,   GSDMD?,1,   GSDMD↓,1,   GSH↑,1,   GSH∅,1,   p‑GSK‐3β↑,1,   GSR↑,2,   GSSG↓,1,   GutMicro↑,1,   hepatoP↑,1,   HEY1↑,1,   HGF/c-Met↑,1,   HIF-1↓,1,   Hif1a↑,2,   Hif1a∅,2,   HIF2a↑,1,   HK2↑,2,   HO-1↑,1,   HSP70/HSPA5↑,4,   HSPs↑,1,   IL1↓,1,   IL1↑,1,   IL10↑,4,   IL1β↓,5,   IL2↑,1,   IL6↓,4,   IL6↑,1,   IL8↓,1,   Inflam↓,15,   iNOS↓,1,   iNOS↑,1,   Insulin↓,1,   ITGB1↑,1,   p‑JNK↑,1,   Keap1↓,1,   lactateProd↓,1,   LDH↓,1,   LDHB↑,1,   MAPK↑,2,   MCP1↑,1,   MDA↓,4,   memory↑,1,   miR-34b-5p↓,1,   mitResp↓,1,   MMP↑,1,   MMP↝,1,   MMP∅,1,   MMP2↑,2,   MMP9↓,1,   MMP9↑,1,   MMPs↑,1,   motorD↑,4,   MPT↑,1,   MSCs↑,1,   mTOR↓,1,   mTOR↑,2,   NAD↑,1,   necrosis↓,1,   neuroP↑,3,   NF-kB↓,3,   NLRP3↓,2,   NO↓,2,   NO↑,1,   NOTCH↑,1,   NRF2↑,2,   OCN↑,1,   OPN↑,1,   other?,1,   other↓,1,   other↑,6,   other↝,1,   OXPHOS↓,2,   OXPHOS↑,2,   p38↑,2,   p‑P70S6K↑,1,   Pain↓,3,   PDGF↑,1,   PFKL↑,2,   PFKM↑,2,   PFKP↑,1,   PGC-1α↑,2,   PGE2↓,2,   pH↑,1,   PI3K↑,1,   PKA↑,1,   PKCδ↓,1,   PKM2↑,2,   PONs↓,1,   PPP↓,1,   QoL↑,2,   ROS↓,12,   ROS↑,3,   mt-ROS↑,1,   RUNX2↑,1,   selectivity↑,1,   SMAD4↑,1,   SMAD5↑,1,   SOD↑,6,   SOD1↑,3,   SOD2↓,1,   SOD2↑,2,   SOX9↑,1,   SREBP1↓,1,   STAC2↑,1,   STAT3↓,2,   p‑STAT3↓,1,   TCA↑,1,   TGF-β↑,2,   TIMP1↑,1,   TNF-α↓,6,   TNF-α↑,1,   toxicity?,1,   toxicity↓,4,   toxicity∅,4,   Trx↓,1,   TumCG↑,1,   TumCMig↑,1,   tumCV↑,1,   VEGF↓,1,   VEGF↑,9,   VEGFR2↑,1,   VGCC↑,1,   Wnt↑,2,   YAP/TEAD↑,1,   β-catenin/ZEB1↑,3,  
Total Targets: 182

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

 

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