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Pulsed electromagnetic fields inhibit atherosclerosis by regulating pyroptosis through membrane tension-mediated

Hongxin Cheng1,2, Qing Zhang1,2, Wen Zhong1,2

  • 1Department of Rehabilitation Medicine Center and Institute of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Signal Transduction and Targeted Therapy
|November 27, 2025
PubMed

Insights

Pulsed electromagnetic fields (PEMFs) show promise for treating atherosclerosis by reducing inflammation and pyroptosis. This noninvasive therapy targets endothelial cell dysfunction, offering a new approach for cardiovascular disease.

Area of Science:

  • Cardiovascular Science
  • Biomedical Engineering
  • Cell Biology

Background:

  • Atherosclerosis is a major cause of cardiovascular diseases, with current treatments having limitations.
  • Endothelial cell inflammation and pyroptosis are key features of atherosclerosis progression.
  • Novel therapeutic strategies are needed to address the unmet needs in atherosclerosis treatment.

Purpose of the Study:

  • To investigate the therapeutic potential of pulsed electromagnetic fields (PEMFs) in treating atherosclerosis.
  • To elucidate the underlying mechanisms of PEMF action on endothelial cells and atherosclerosis.
  • To explore PEMFs as a noninvasive treatment for cardiovascular and arterial diseases.

Main Methods:

  • Utilized ApoE-/- and ApoE-/-NLRP3-/- knockout mice models.
  • Conducted experiments on human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs).
  • Performed proteomic analysis on plasma samples from atherosclerosis patients and mechanistic studies involving mitochondrial function and TRPV4 channels.

Main Results:

  • PEMFs effectively inhibited NLRP3 inflammasome activation, reduced atherosclerotic plaque formation, and delayed disease progression.
  • Significant endothelial cell inflammation and pyroptosis were observed during atherosclerosis.
  • PEMFs improved mitochondrial dysfunction in endothelial cells by regulating membrane tension and TRPV4 channels, reducing pyroptosis.

Conclusions:

  • PEMFs represent a promising noninvasive therapeutic strategy for atherosclerosis.
  • The study reveals a novel mechanobiological pathway involving membrane tension, TRPV4 channels, and mitochondrial function in PEMF treatment.
  • Findings provide a theoretical basis for developing PEMF-based therapies for atherosclerosis and related inflammatory diseases.

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