ArticleMediators of inflammation2024
Electroacupuncture Improves Cardiac Function via Inhibiting Sympathetic Remodeling Mediated by Promoting Macrophage M2 Polarization in Myocardial Infarction Mice.
Article in Mediators of inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Electroactive Biomaterials for Cardiovascular Tissue Engineering: Mechanisms, Design Strategies, and Therapeutic Applications.Journal of functional biomaterials · 2026Review
- Hyperoside Alleviates Myocardial Fibrosis by Reducing Oxidative Stress via the GATA4/HIF-1α Pathway in Mice.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Review
- Article
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Electroacupuncture Protects Against Post-MI Heart Failure Through Autonomic Regulation and α7nAChR Activation.Cardiology research and practice · 2026Article
- Effects of Long-Term Moderate-Intensity Exercise on Autonomic Nervous System Dysfunction Induced by Cardiac Neurovascular Interface Deterioration.Reviews in cardiovascular medicine · 2025Review
- Nourishment of Nerves and Innervation: A Novel Approach for the Treatment of Myocardial Infarction.Cardiology · 2025Review
- Neural mechanism of HT7 electroacupuncture in myocardial ischemia: critical role of the paraventricular nucleus oxytocin system.Frontiers in neuroscience · 2025Article
- Electroacupuncture Improves Ovarian Function in Rats WithMediators of inflammation · 2025Article
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Authors and funding
10 authors.
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Abstract
Electroacupuncture (EA) at the Neiguan acupoint (PC6) has shown significant cardioprotective effects. Sympathetic nerves play an important role in maintaining cardiac function after myocardial infarction (MI). Previous studies have found that EA treatment may improve cardiac function by modulating sympathetic remodeling after MI. However, the mechanism in how EA affects sympathetic remodeling and improves cardiac function remains unclear. The aim of this study is to investigate the cardioprotective mechanism of EA after myocardial ischemic injury by improving sympathetic remodeling and promoting macrophage M2 polarization. We established a mouse model of MI by occluding coronary arteries in male C57/BL6 mice. EA treatment was performed at the PC6 with current intensity (1 mA) and frequency (2/15 Hz). Cardiac function was evaluated using echocardiography. Heart rate variability in mice was assessed via standard electrocardiography. Myocardial fibrosis was evaluated by Sirius red staining. Levels of inflammatory factors were assessed using RT-qPCR. Sympathetic nerve remodeling was assessed through ELISA, western blotting, immunohistochemistry, and immunofluorescence staining. Macrophage polarization was evaluated using flow cytometry. Our results indicated that cardiac systolic function improved significantly after EA treatment, with an increase in fractional shortening and ejection fraction. Myocardial fibrosis was significantly mitigated in the EA group. The sympathetic nerve marker tyrosine hydroxylase and the nerve sprouting marker growth-associated Protein 43 were significantly reduced in the EA group, indicating that sympathetic remodeling was significantly reduced. EA treatment also promoted macrophage M2 polarization, reduced levels of inflammatory factors TNF-
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