Cited by 7Cardiac Fibrosis and RemodelingElectromagnetic Fields and Biological EffectsCardiac Ischemia and Reperfusion

Pulsed electromagnetic fields treatment ameliorates cardiac function after myocardial infarction in mice and pigs

Open access
Wang, Shiqi, Pei, Gaiqin, Shen, Jiayu, Fang, Zhi, Chen, Tingyu, Wang, Lu, Cheng, Hongxin, Li, Hanbin +7 more·2026·Journal of Advanced Research

Abstract

• PEMF treatment can ameliorate cardiac function and reduce scar size in post-MI mice and pigs. • The benefits of PEMF in the treatment of MI are supported by reduced inflammatory responses, improved cell survival, and decreased collagen secretion. • The underlying molecular mechanism of PEMF treatment is associated with the inhibition of the TLR4/MyD88/NF-κB and TGF-β1/SMAD3 signaling pathways. • From the perspective of safety, the process of PEMF treatment is safe. No adverse events occur. PEMF treatment does not cause damage to liver or kidney function and does not lead to the growth of harmful intestinal flora. • PEMF treatment holds significant promise as a noninvasive physical therapy modality, justifying further exploration of its potential implications for managing patients with IHD. Ischemic heart disease (IHD) is a prominent contributor to mortality worldwide, with myocardial infarction (MI) representing its most severe manifestation. Pulsed electromagnetic fields (PEMF) treatment shows promise for treating IHD. Nevertheless, the therapeutic impact and underlying mechanism of PEMF in MI are not fully understood. To investigate the efficacy, safety, and mechanisms of PEMF for MI. We established MI models in both mice and pigs and performed serial echocardiography and cardiac magnetic resonance follow-up to demonstrate the benefit of PEMF treatment after MI. The pathological environment after myocardial infarction was simulated in vitro to observe changes in various cells exposed to PEMF. Gene knockout (TLR4 -/- ) mice and inhibitors were used to compare the differences in the efficacy of PEMF treatment relative to that of gene knockout/inhibitor treatments. Agonists were used to further explore the mechanism of PEMF treatment. In post-MI mice, PEMF treatment enhanced cardiac function and reduced scar formation. PEMF reduced the macrophage inflammatory response, improved cardiomyocyte survival in an inflammatory environment, and decreased collagen secretion by fibroblasts in vitro . Importantly, in the clinically relevant porcine model, PEMF treatment inhibited the inflammatory response and alleviated adverse left ventricular remodeling. Moreover, PEMF could exert therapeutic effects similar to those of gene knockout or inhibitor treatments. In the presence of TLR4 knockout or pyrrolidine dithiocarbamate (an NF-κB inhibitor) administration, PEMF could still improve cardiac function in post-MI mice. Mechanistically, the anti-inflammatory effect of PEMF was reversed when RS09 (a TLR4 agonist) was administered, and the antifibrotic effect of PEMF was attenuated after treatment with SRI-011381 (a TGF-β signaling pathway agonist). PEMF treatment exhibits considerable promise as a noninvasive physical therapy modality, warranting further investigation into its potential implications for managing patients with IHD.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.jare.2025.04.019

Cites

66 of 66 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • PEMF therapy has cardioprotective and neuroprotective potential via enhancing cell survival, reducing inflammation and fibrosis, and promoting vascular repair and neuroplasticity.

    “Pulsed electromagnetic field (PEMF) therapy has demonstrated cardioprotective and neuroprotective potential via enhancing cell survival, reducing inflammation and fibrosis and promoting vascular repair and neuroplasticity [7,8,9,10].”

    From The Heart’s Electromagnetic Field in Emotions, Empathy and Human Connection: Biosensor-Derived Insights into Heart–Brain Axis Mechanisms and a Basis for Novel BioMagnetoTherapies (2026) · cites this paper as [7]

    The Discussion and Conclusions (pages not provided) report improved cardiac function after myocardial infarction, reduced inflammation and fibrosis, and improved cell survival. The Introduction reports angiogenesis in post-MI mice from an earlier study. This paper does not establish neuroprotective effects or neuroplasticity, so it supports only the cardiac and vascular portions of the sentence. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • In preclinical models of myocardial infarction and ischemia-reperfusion injury, PEMF improves cardiac function, limits remodeling, and enhances angiogenesis.

    “In preclinical models of myocardial infarction and ischemia–reperfusion injury, PEMF improved cardiac function, limited remodeling and enhanced angiogenesis [7,8,9,148].”

    From The Heart’s Electromagnetic Field in Emotions, Empathy and Human Connection: Biosensor-Derived Insights into Heart–Brain Axis Mechanisms and a Basis for Novel BioMagnetoTherapies (2026) · cites this paper as [7]

    The Conclusions and Discussion report improved cardiac function and reduced scar formation or adverse remodeling after PEMF treatment in post-MI mice and pigs. The Introduction reports angiogenesis in post-MI mice from the authors’ previous studies. This paper’s models used permanent coronary ligation, so it does not support extending these findings to ischemia–reperfusion injury. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Wang, S., Pei, G., Shen, J., Fang, Z., Chen, T., Wang, L., Cheng, H., Li, H., Pei, H., Feng, Q., Fan, Q., He, C., Fu, C., Guo, Y., & Wei, Q.
Affiliations
Sichuan University (CN)
Corresponding author
  • Fu, Chenying
  • Guo, Yingqiang
  • Wei, Quan
Venue
Journal of Advanced Research
Publisher
Elsevier BV
Published
2026-02
Volume
80
Pages
1139-1153
ISSN
  • 2090-1224 (ISSN-L)
  • 2090-1232
OpenAlex
W4409499315
Cited by
6
References
66
Citations by year
2026: 3 · 2025: 3
FWCI
4.17
Type
journal article
Language
en
Open access
Locations
  • Journal of Advanced Research (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • Natural Science Foundation of Sichuan Province (2023NSFSC1495, 2023NSFSC1999, 2023NSFSC1654)
  • National Natural Science Foundation of China (82372574, 82202793, 82172534)
  • Sichuan University (ZYJC21038, JH20231160)
  • China Postdoctoral Science Foundation (2023M732452, 2023SCUH0048)
  • West China Hospital, Sichuan University
  • National Key Research and Development Program of China (2023YFC3603800, 2023YFC3603801)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biophysics › Electromagnetic Fields and Biological Effects
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
Keywords
pulsed electromagnetic fields, myocardial infarction, cardiac function, cardiac remodeling, myocardial scar formation, inflammation, cardiomyocyte survival, TLR4/MyD88/NF-κB signaling, TGF-β1/Smad3 signaling, anti-inflammatory therapy, antifibrotic therapy, ischemic heart disease, porcine model
MeSH terms
Animals, Disease Models, Animal, Echocardiography, Electromagnetic Fields, Male, Mice, Inbred C57BL, Myocardial Infarction, Swine, Mice, Knockout, Ventricular Remodeling, Myocytes, Cardiac, Toll-Like Receptor 4, Mice, Magnetic Field Therapy

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review