2026 年第 3 期 第 21 卷

线粒体自噬在心肌缺血再灌注损伤中的研究进展

Research progress of mitophagy in myocardial ischemia-reperfusion injury

作者：邹振飞1莫桂熙2

英文作者：Zou Zhenfei1 Mo Guixi2

单位：1广东医科大学第一临床医学院，湛江524023；2广东医科大学附属医院麻醉手术中心，湛江524023

英文单位：1The First School of Clinical Medicine Guangdong Medical University Zhanjiang 524023 China; 2Anesthesiology and Surgery Center Affiliated Hospital of Guangdong Medical University Zhanjiang 524023 China

关键词：心肌缺血再灌注损伤；线粒体自噬；细胞自噬；氧化应激

英文关键词：Myocardialischemia-reperfusioninjury;Mitophagy;Autophagy;Oxidativestress

• 摘要：

• 心肌缺血再灌注损伤(MIRI)是心血管疾病中常见且严重的病理过程，常导致心肌细胞的损伤与功能障碍。近年来，线粒体自噬这一重要的细胞自噬机制逐渐受到学术界的广泛关注。线粒体自噬不仅在维持细胞内线粒体稳态方面发挥关键作用，还在MIRI的过程中影响细胞存活、能量代谢及氧化应激反应。已有研究表明线粒体自噬通过清除受损线粒体来促进心肌细胞的生存与功能恢复，但其具体机制仍需进一步探讨。本文旨在综述线粒体自噬在MIRI中的最新研究进展，分析其对心肌细胞生存及代谢的影响，及其在氧化应激中的作用，以期为未来研究提供参考和指导。

• 】Myocardial ischemia-reperfusion injury (MIRI) is a common and severe pathological process in cardiovascular diseases, which often leads to cardiomyocyte damage and dysfunction. In recent years, mitophagy, an important cellular autophagic mechanism, has attracted extensive attention in academic circles. Mitophagy not only plays a key role in maintaining intracellular mitochondrial homeostasis, but also affects cell survival, energy metabolism and oxidative stress response during MIRI. Existing studies have shown that mitophagy promotes cardiomyocyte survival and functional recovery by clearing damaged mitochondria, but its specific mechanism still needs further exploration. This article aims to review the latest research progress of mitophagy in MIRI, analyze its effects on cardiomyocyte survival and metabolism as well as its role in oxidative stress, so as to provide reference and guidance for future research.