线粒体自噬对缺血性脑卒中的作用及其机制研究进展  

Research advances in the role and mechanism of mitophagy in ischemic stroke

作　　者：李婷婷 王钦鹏[2] 刘晓庆 蔡珂 魏阳阳(综述) 梁成(审校)[2] LI Tingting;WANG Qinpeng;LIU Xiaoqing(The Second Clinical Medical College of Lanzhou University,Lanzhou 730030,China)

机构地区：[1]兰州大学第二临床医学院,甘肃兰州730030 [2]兰州大学第二医院神内ICU,甘肃兰州730030

出　　处：《中风与神经疾病杂志》2024年第1期41-46,共6页Journal of Apoplexy and Nervous Diseases

基　　金：甘肃省科技厅自然科学基金(20210405JCC1549);甘肃省神经病学重点实验室(20JR10RA766)。

摘　　要：线粒体自噬作为一种选择性自噬,是线粒体质量控制的关键机制之一。脑组织缺血可引发多种分子的级联反应,导致功能障碍线粒体的堆积。线粒体功能障碍可诱导线粒体自噬的激活,通过清除受损或去极化线粒体来维持神经元细胞的稳态。研究表明线粒体自噬与缺血性脑卒中的病理过程密切相关,但其具体机制及其作用一直备受争议。本文就线粒体自噬的发生机制及其在缺血脑组织中的作用进行综述,为临床治疗缺血性脑卒中提供新的思路。As a type of selective autophagy,mitophagy is one of the key mechanisms for mitochondrial quality control.Cerebral ischemia can trigger a variety of molecular cascade reactions,resulting in the accumulation of dysfunctional mitochondria.Mitochondrial dysfunction can induce the activation of mitophagy and maintain the homeostasis of neuronal cells by clearing damaged or depolarized mitochondria.Studies have shown that mitophagy is closely associated with the pathological process of ischemic stroke,but there are still controversies over its specific mechanism and role.This article reviews the mechanism of mitophagy and its role in ischemic brain tissue,so as to provide new ideas for the clinical treatment of ischemic stroke.

关 键 词：脑缺血缺氧 线粒体自噬 炎症反应 氧化应激 程序性细胞死亡 

分 类 号：R743[医药卫生—神经病学与精神病学]