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.
作者
李婷婷
王钦鹏
刘晓庆
蔡珂
魏阳阳(综述)
梁成(审校)
LI Tingting;WANG Qinpeng;LIU Xiaoqing(The Second Clinical Medical College of Lanzhou University,Lanzhou 730030,China)
出处
《中风与神经疾病杂志》
CAS
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)。
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
Cerebral ischemia and hypoxia
Mitophagy
Inflammatory response
Oxidative stress
Programmed cell death
