中国药物警戒 ›› 2025, Vol. 22 ›› Issue (12): 1328-1333.
DOI: 10.19803/j.1672-8629.20250781

• 心脑血管中药作用机制与安全性评价专栏 • 上一篇    下一篇

中医药调控线粒体稳态改善心肌梗死研究进展

白雪1, 李京宬2, 李雪丽1*   

  1. 1中国中医科学院医学实验中心,北京市中医药防治重大疾病基础研究重点实验室,北京 100700;
    2新加坡南洋理工大学,新加坡 639798
  • 收稿日期:2025-11-05 发布日期:2025-12-19
  • 通讯作者: *李雪丽,女,博士,副研究员,中药防治心脑血管疾病。E-mail: emilia1801@qq.com
  • 作者简介:白雪,女,博士,助理研究员,中药防治心脑血管疾病。
  • 基金资助:
    国家自然科学基金资助项目（82204670、82304767）; 中央级公益性科研院所基本科研业务费专项基金（ZZ13-YQ-081、ZZ15-YQ-055、XTCX2023002）; 中国中医科学院科技创新工程项目（CI2021B017）

Research Advances in Roles of Traditional Chinese Medicine in Improving Myocardial Infarction by Regulating Mitochondrial Homeostasis

BAI Xue1, LI Jingcheng2, LI Xueli1*   

  1. 1Experimental Research Center, China Academy of Chinese Medical Sciences, Beijing Key Laboratory of Traditional Chinese Medicine Basic Research on Prevention and Treatment of Major Disease, Beijing 100700, China;
    2Nanyang Technological University, 639798, Singapore
  • Received:2025-11-05 Published:2025-12-19

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摘要： 目的 分析线粒体稳态病理改变在心肌梗死（Myocardial Infarction,MI）进展中的作用,系统阐述中医药调控线粒体稳态改善MI的最新研究进展,以期为基于线粒体保护途径防治MI提供参考。方法 通过检索归纳近年来MI与线粒体稳态的相关文献,系统分析线粒体稳态失衡在MI中的核心病理作用,并总结中医药通过多靶点作用调控线粒体功能改善MI的实验研究进展。结果 近年研究证实,线粒体稳态失衡是MI的核心病理机制,表现为氧化磷酸化功能障碍、ROS爆发和Ca2+超载、膜通透性转换、线粒体动力学异常、线粒体自噬失调和线粒体途径细胞死亡的激活等;针对心肌线粒体内稳态紊乱及由此引发的线粒体网络自我更新和质量控制体系稳态失衡,中药复方、单味药以及活性成分表现出多层次、多途径和多靶点的协同改善作用,可减轻线粒体损伤,维持线粒体稳态,减少心肌细胞凋亡,改善心脏功能和延缓心室重构。结论 线粒体稳态失衡是MI进展的核心病理环节,中医药通过多成分多靶点协同调控线粒体稳态展现出心肌保护潜力,为开发基于线粒体保护的MI防治新策略提供参考。

关键词: 心肌梗死, 线粒体稳态, 中医药, 线粒体质量控制, 病理机制

Abstract: Objective To analyze the roles of pathological changes in mitochondrial homeostasis during the progression of myocardial infarction (MI), and to summarize the latest research advances in improving MI by traditional Chinese medicine (TCM) via the regulation of mitochondrial homeostasis in order to provide data for prevention and treatment of MI through mitochondrial protective pathways. Methods Recent literature on MI and mitochondrial homeostasis was retrieved before the core pathological roles of mitochondrial homeostatic imbalance in MI were analyzed and advances in experimental studies on the ability of TCM to improve MI by regulating mitochondrial function through multi-target mechanisms were outlined. Results Recent studies suggested that mitochondrial homeostatic imbalance was a major pathological mechanism for MI, which manifested itself in impaired oxidative phosphorylation, ROS burst, Ca2+ overload, mitochondrial permeability transition, abnormal mitochondrial dynamics, dysregulated mitophagy, and mitochondria-mediated activation of cell death pathways. By targeting abnormal mitochondrial homeostasis in cardiomyocytes and the consequent imbalance of both mitochondrial network remodeling and the mitochondrial quality control system, TCM formulas, single herbs, and active compounds could exert multilevel, multi-pathway, and multitarget synergistic effects that helped alleviate mitochondrial injury, maintain mitochondrial homeostasis, reduce cardiomyocyte apoptosis, improve myocardial function, and attenuate ventricular remodeling. Conclusion Mitochondrial homeostatic imbalance is pathologically critical to MI progression. TCM has a cardioprotective potential by regulating mitochondrial homeostasis through multicomponent, multitarget actions. This study is expected to provide insights into MI prevention and treatment strategies based on mitochondrial protection.

Key words: Myocardial Infarction, Mitochondrial Homeostasis, Traditional Chinese Medicine, Mitochondrial Quality Control, Pathological Mechanisms

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