condition found tbRes List
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↓, 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


VEGF, Vascular endothelial growth factor: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
A signal protein produced by many cells that stimulates the formation of blood vessels. Vascular endothelial growth factor (VEGF) is a signal protein that plays a crucial role in angiogenesis, the process by which new blood vessels form from existing ones. This process is vital for normal physiological functions, such as wound healing and the menstrual cycle, but it is also a key factor in the growth and spread of tumors in cancer.
Because of its significant role in tumor growth and progression, VEGF has become a target for cancer therapies. Anti-VEGF therapies, such as monoclonal antibodies (e.g., bevacizumab) and small molecule inhibitors, aim to inhibit the action of VEGF, thereby reducing blood supply to tumors and limiting their growth. These therapies have been used in various types of cancer, including colorectal, lung, and breast cancer.
Scientific Papers found: Click to Expand⟱
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)

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↑,

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

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.

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.

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

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

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↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Results for Effect on Cancer/Diseased Cells:
angioG↓,1,   angioG↑,1,   Apoptosis↑,2,   Ca+2↑,2,   Ca+2↝,1,   CSCs↓,1,   eff↓,1,   eff↝,1,   LIF↑,1,   MAPK↑,1,   Necroptosis↑,1,   NO↑,1,   p38↑,1,   RadioS↑,1,   ROS↑,3,   selectivity↑,2,   Slug↓,1,   p‑SMAD2↓,1,   p‑SMAD3↓,1,   TGF-β↓,1,   TumCCA↑,1,   TumCI↓,1,   TumCMig↓,1,   TumCP↓,2,   Twist↓,1,   VEGF↓,1,   VEGF↑,1,   VGCC↑,1,   Vim↓,1,   β-catenin/ZEB1↓,2,  
Total Targets: 30

Results for Effect on Normal Cells:
Akt↓,1,   Akt↑,1,   p‑Akt↑,1,   angioG↑,3,   angioG↝,1,   Apoptosis↓,1,   ATP↑,1,   BAD↓,1,   BAX↓,1,   Bcl-xL↑,1,   BMP2↑,1,   BMPs↓,1,   Ca+2↓,1,   Ca+2↑,3,   cardioP↑,1,   Casp3↓,1,   COL2A1↑,1,   Diff↑,2,   E2Fs↑,1,   eff↓,1,   eff↑,3,   ERK↑,1,   p‑ERK↑,1,   FAK↑,1,   FGF↑,2,   HGF/c-Met↑,1,   HIF-1↓,1,   Hif1a↑,2,   Hif1a∅,1,   HSP70/HSPA5↑,1,   IL1↑,1,   IL10↑,2,   IL1β↓,1,   IL2↑,1,   IL6↓,1,   Inflam↓,3,   ITGB1↑,1,   MAPK↑,1,   memory↑,1,   MMP2↑,1,   MMP9↓,1,   MMP9↑,1,   MMPs↑,1,   MSCs↑,1,   mTOR↓,1,   mTOR↑,1,   neuroP↑,1,   NF-kB↓,1,   NO↓,2,   other↑,2,   p38↑,1,   PDGF↑,1,   PGE2↓,1,   PKA↑,1,   PKCδ↓,1,   ROS↓,2,   ROS↑,1,   SMAD4↑,1,   SMAD5↑,1,   SOD↑,1,   SOX9↑,1,   TGF-β↑,1,   TIMP1↑,1,   TNF-α↓,1,   TNF-α↑,1,   toxicity∅,2,   VEGF↓,1,   VEGF↑,9,   VEGFR2↑,1,   Wnt↑,1,   β-catenin/ZEB1↑,1,  
Total Targets: 71

Scientific Paper Hit Count for: VEGF, Vascular endothelial growth factor
11 Magnetic Fields
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:334  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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