Mitophagy in Ischaemia/Reperfusion Induced Cerebral Injury

被引:38
|
作者
Liu, Kangyong [1 ,2 ]
Sun, Yinyi [2 ]
Gu, Zhaohua [1 ]
Shi, Nan [1 ]
Zhang, Ting [2 ]
Sun, Xiaojiang [2 ]
机构
[1] Shanghai Pudong New Area Zhoupu Hosp, Dept Neurol, Shanghai, Peoples R China
[2] Shanghai Jiao Tong Univ, Dept Neurol, Affiliated Peoples Hosp 6, Shanghai 200233, Peoples R China
基金
中国国家自然科学基金;
关键词
Autophagy; Mitophagy; Ischaemia/reperfusion; Cerebral injury; OXIDATIVE STRESS; CELL-DEATH; MITOCHONDRIAL DYSFUNCTION; AUTOPHAGY; MECHANISMS; RAPAMYCIN; PROTEIN; DEGRADATION; ISCHEMIA; PHOSPHORYLATION;
D O I
10.1007/s11064-013-1033-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondrial autophagy (Mitophagy), the specific autophagic elimination of mitochondria, has been related with several forms of degenerative disease and mitochondrial dysfunction. It is involved in multiple cellular processes. In addition to one of its established key roles in the maintenance of normal cellular phenotype and function, there is growing interest in the concept that targeted modulation of mitophagy may reduce cerebral ischaemia/reperfusion injury. Induction of mitophagy results in selective clearance of damaged mitochondria in cells. In response to stress such as ischaemia/reperfusion, prosurvival and prodeath pathways are concomitantly activated in neuronal cells.
引用
收藏
页码:1295 / 1300
页数:6
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