线粒体自噬在心肌缺血再灌注损伤中的机制

doi:10.16138/j.1673-6087.2024.05.08

摘要/Abstract

摘要：

心血管疾病仍然是世界上最常见的死亡原因之一，在过去，及时的再灌注治疗大大减少了疾病死亡率，同时促进了血液的恢复和心肌细胞的复苏。缺血再灌注（ischemia reperfusion， IR）损伤是许多临床实践中不可避免的病理过程，心肌IR损伤的机制包括线粒体自噬、细胞凋亡等多种病理过程，这些信号通路相互关联和作用。其中，线粒体自噬作为一种选择性自噬受到广泛关注，通过调节线粒体的质量与数量维持心肌细胞的正常运行，但当受到氧化应激、缺血、缺氧等刺激时，过度的线粒体自噬或线粒体自噬不足均可影响心肌细胞功能，甚至导致心肌细胞死亡，因此应严格控制心肌细胞中线粒体自噬的激活程度。故本文就线粒体自噬在心肌IR损伤中的机制及进展作一综述，旨在能够为心肌IR损伤的研究提供一些助力。

关键词: 自噬, 线粒体自噬, 缺血再灌注损伤

Abstract:

Cardiovascular disease is still one of the most common causes of death in the world. In the past, timely reperfusion treatment has greatly reduced the death rate of the disease while promoting blood recovery and cardiomyocyte recovery. Ischemia reperfusion (IR) injury is an inevitable pathological process in many clinical practices. The mechanisms of myocardial IR injury include a variety of pathological processes such as mitochondrial autophagy and apoptosis, and these signaling pathways are interrelated and act on each other. Among them, mitochondrial autophagy has attracted wide attention as a selective autophagy. Mitochondrial autophagy maintains the normal operation of cardiomyocytes by regulating the quality and quantity of mitochondria. However, as stimulated by oxidative stress, ischemia and hypoxia, excessive mitochondrial autophagy or insufficient mitochondrial autophagy can affect the function of cardiomyocytes and even lead to the death of cardiomyocytes. Therefore, the activation degree of mitochondrial autophagy in cardiomyocytes should be strictly controlled. This article reviews the mechanism and progress of mitochondrial autophagy in myocardial IR injury, aiming to provide some assistance in the study of myocardial IR injury.

Key words: Autophagy, Mitochondrial autophagy, Ischemia reperfusion injury

中图分类号:

R542.2

高悦, 幸世峰. 线粒体自噬在心肌缺血再灌注损伤中的机制[J]. 内科理论与实践, 2024, 19(05): 328-332.

GAO Yue, XING Shifeng. Mechanism of mitochondrial autophagy in myocardial ischemia-reperfusion injury[J]. Journal of Internal Medicine Concepts & Practice, 2024, 19(05): 328-332.

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