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Electroacupuncture Protects Against Post-MI Heart Failure Through Autonomic Regulation and α7nAChR Activation
Weiting Wang1,2, Jiaojiao Wu1,2, Yueling Xu1,2
1Acupuncture Anaesthesia Clinical Research Institute, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China, shutcm.edu.cn.
Cardiology Research and Practice
|June 25, 2026
Summary
Electroacupuncture (EA) at the Neiguan (PC6) acupoint improves heart function after myocardial infarction (MI) by activating the vagus nerve and downstream signaling pathways. This neuro-immune-angiogenic mechanism promotes myocardial repair.
Area of Science:
- Cardiovascular Research
- Neuroscience
- Integrative Medicine
Background:
- Myocardial infarction (MI) often leads to adverse cardiac remodeling and heart failure (HF).
- The vagus nerve-mediated cholinergic pathway plays a crucial role in regulating cardiovascular function and inflammation.
- Understanding the molecular mechanisms underlying neuro-modulatory interventions for post-MI HF is essential for developing effective treatments.
Purpose of the Study:
- To investigate if electroacupuncture (EA) at the Neiguan (PC6) acupoint can alleviate adverse myocardial remodeling in post-MI HF.
- To determine if EA activates the vagus nerve-mediated cholinergic pathway and its downstream signaling cascade (α7nAChR-Akt-HIF-1α-VEGF).
Main Methods:
- Male Sprague Dawley rats were used, with groups including sham, MI model, and EA treatment.
- MI was induced surgically, and EA was applied at PC6 for 14 days post-MI.
- Cardiac function, structure, and molecular markers (ChAT, α7nAChR, p-Akt, HIF-1α, VEGF) were assessed using echocardiography, histology, qPCR, Western blotting, and immunohistochemistry.
Main Results:
- EA intervention significantly attenuated pathological myocardial remodeling and improved cardiac function in post-MI rats.
- EA treatment enhanced cardiac contractility, reduced ventricular dilation, restored autonomic balance, and alleviated myocardial necrosis and fibrosis.
- Molecular analysis showed EA increased choline acetyltransferase (ChAT) and α7-nicotinic acetylcholine receptor (α7nAChR) expression, elevated phosphorylated Akt (p-Akt), and upregulated hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF).
Conclusions:
- EA effectively attenuated maladaptive ventricular remodeling and improved cardiac performance post-MI.
- These beneficial effects are associated with the modulation of autonomic function and activation of the α7nAChR/Akt/HIF-1α/VEGF signaling axis.
- The findings support a potential neuro-immune-angiogenic mechanism for EA-mediated myocardial repair in the subacute post-MI phase.
