Mechanism of mitochondrial autophagy in myocardial ischemia-reperfusion injury

doi:10.16138/j.1673-6087.2024.05.08

Abstract

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

CLC Number:

R542.2

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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