自噬在心肌缺血再灌注损伤中的研究进展  

The research progress of autophagy in myocardial ischemia-reperfusion injury

作　　者：田国卫[1] 夏豪[1] TIAN Guowei;XIA Hao(Department of Cardiology,Renmin Hospital of Wuhan University,Wuhan 430060,China)

机构地区：[1]武汉大学人民医院心内科,430060

出　　处：《疑难病杂志》2018年第10期1179-1184,共6页Chinese Journal of Difficult and Complicated Cases

基　　金：国家自然科学基金(81270184)

摘　　要：自噬是在细胞内清除功能不全的细胞器和长寿蛋白质,从而保证细胞内稳态平衡。正常情况下,心肌细胞自噬维持在较低的水平。当心肌细胞在缺血缺氧状态时,受能力缺乏和氧化应激的影响,细胞的自噬水平会上调。通过回收利用细胞内衰老的细胞器及错误折叠的蛋白质来满足细胞对能量的需求从而保护心肌细胞。而多项研究发现缺血心肌再灌注时,自噬水平被过度激发,加速心肌细胞的死亡。在此,着重讨论自噬在心肌缺血再灌注过程中所起的作用,并试述其潜在的信号通路。Autophagy is the removal of dysfunctional organelles and long-lived proteins within the cell, thus ensuring homeostasis in the cell. Under normal circumstances, myocardial cell autophagy is maintained at a low level. When the eardio- myoeytes are under hypoxie conditions, they are affected by the lack of ability and oxidative stress, and the autophagy level of the cells is upregulated. By reusing intraeellular senescent organelles and misfolded proteins to meet the energy needs of cells to protect eardiomyoeytes. A number of studies have found that autoinmmne levels are excessively stinmlated during isehemie reperfusion and accelerate myocardial cell death. In this review,we will focus on the role of autophagy in the process of myocar- dial isehemia and reperfusion, and describe its potential signaling pathways.

关 键 词：自噬 心肌缺血再灌注 综述 

分 类 号：R54[医药卫生—心血管疾病]