2. Academic Validation
  3. Pulsed electromagnetic fields inhibit atherosclerosis by regulating pyroptosis through membrane tension-mediated mechanosensitive channels

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

  • Signal Transduct Target Ther. 2025 Nov 28;10(1):388. doi: 10.1038/s41392-025-02479-2.
Hongxin Cheng # 1 2,  Qing Zhang # 1 2,  Wen Zhong 1 2,  Hanbin Li 1 2,  Lu Wang 1 2,  Shiqi Wang 1 2,  Chengqi He 1 2,  Chenying Fu 3 4,  Quan Wei 5 6
Affiliations

Affiliations

  • 1 Department of Rehabilitation Medicine Center and Institute of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
  • 2 Key Laboratory of Rehabilitation Medicine in Sichuan Province, Chengdu, Sichuan, China.
  • 3 State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan, China. [email protected].
  • 4 Geriatric Health Care and Medical Research Center, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan, China. [email protected].
  • 5 Department of Rehabilitation Medicine Center and Institute of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China. [email protected].
  • 6 Key Laboratory of Rehabilitation Medicine in Sichuan Province, Chengdu, Sichuan, China. [email protected].
  • # Contributed equally.
PMID: 41309549 DOI: 10.1038/s41392-025-02479-2
Abstract

Atherosclerosis serves as the core pathological basis of cardiovascular, cerebrovascular, and peripheral arterial diseases, posing a serious threat to human health. However, current mainstream treatments such as statin drugs and stent implantation are associated with significant side effects or limited efficacy, highlighting the urgent need for new therapeutic strategies. Pulsed electromagnetic fields (PEMFs), due to their noninvasive nature and anti-inflammatory properties, show potential in the treatment of atherosclerosis. This study utilized ApoE-/- mice, ApoE-/-NLRP3-/- knockout mice, human umbilical vein endothelial cells (HUVECs), human aortic endothelial cells (HAECs), and human plasma samples for experiments, revealing significant endothelial cell (EC) inflammation and Pyroptosis during the progression of atherosclerosis. PEMFs were found to effectively inhibit the activation of the NLRP3 inflammasome, reduce plaque formation, and delay the progression of atherosclerosis. Proteomic analysis of plasma from atherosclerosis patients further indicated elevated expression levels of proteins related to inflammation and Pyroptosis, with particularly notable changes in membrane proteins. Mechanistic studies demonstrated that PEMFs improve mitochondrial dysfunction in ECs by regulating membrane tension and the mechanosensitive tension-mediated transient receptor potential vanilloid 4 (TRPV4) channels, thereby reducing Pyroptosis. This discovery not only reveals a novel mechanobiological pathway but also provides a solid theoretical foundation for the development of PEMF-based therapies for atherosclerosis. Schematic diagram of the mechanism by which PEMFs treat atherosclerosis (created in BioRender). Wei, B. (2025) https://BioRender.com/undefined ).

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