Mitophagy: mechanisms, pathophysiological roles, and analysis

被引:779
|
作者
Ding, Wen-Xing [1 ]
Yin, Xiao-Ming [2 ]
机构
[1] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66160 USA
[2] Indiana Univ Sch Med, Dept Pathol & Lab Med, Indianapolis, IN 46202 USA
关键词
autophagy; mitophagy; Nix; Parkin; MITOCHONDRIAL PERMEABILITY TRANSITION; UBIQUITIN-PROTEASOME SYSTEM; AUTOPHAGIC CELL-DEATH; M-AAA PROTEASE; PATERNAL MITOCHONDRIA; MEDIATED AUTOPHAGY; OXIDATIVE STRESS; BH3; DOMAIN; DEGRADATION; PARKIN;
D O I
10.1515/hsz-2012-0119
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
Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper cellular functions. Indeed, mitophagy has been recently proposed to play critical roles in terminal differentiation of red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, and ischemia or drug-induced tissue injury. Removal of damaged mitochondria through autophagy requires two steps: induction of general autophagy and priming of damaged mitochondria for selective autophagic recognition. Recent progress in mitophagy studies reveals that mitochondrial priming is mediated either by the Pink 1-Parkin signaling pathway or the mitophagic receptors Nix and Bnip3. In this review, we summarize our current knowledge on the mechanisms of mitophagy. We also discuss the pathophysiological roles of mitophagy and current assays used to monitor mitophagy.
引用
收藏
页码:547 / 564
页数:18
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