How Mitochondrial Dynamism Orchestrates Mitophagy

被引：265

作者：

Shirihai, Orian S. ^{[1
,2
]}

Song, Moshi ^{[3
]}

Dorn, Gerald W., II ^{[3
]}

机构：

[1] Boston Univ, Sch Med, Evans Ctr, Dept Med, Boston, MA 02215 USA

[2] Ben Gurion Univ Negev, Dept Biochem, IL-84105 Beer Sheva, Israel

[3] Washington Univ, Sch Med, Dept Internal Med, Ctr Pharmacogen, St Louis, MO 63110 USA

来源：

CIRCULATION RESEARCH | 2015年 / 116卷 / 11期

基金：

美国国家卫生研究院;

关键词：

autophagy; mitochondria; mitochondrial dynamics; Parkinson disease; PARKIN-MEDIATED MITOPHAGY; DOMINANT OPTIC ATROPHY; E3 UBIQUITIN LIGASE; LOSS-OF-FUNCTION; MITOFUSIN; PINK1-DEPENDENT PHOSPHORYLATION; EMBRYONIC-DEVELOPMENT; DAMAGED MITOCHONDRIA; CARDIAC MITOCHONDRIA; ELECTRON-TRANSPORT;

D O I：

10.1161/CIRCRESAHA.116.306374

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Mitochondria are highly dynamic, except in adult cardiomyocytes. Yet, the fission and fusion-promoting proteins that mediate mitochondrial dynamism are highly expressed in, and essential to the normal functioning of, hearts. Here, we review accumulating evidence supporting important roles for mitochondrial fission and fusion in cardiac mitochondrial quality control, focusing on the PTEN-induced putative kinase 1-Parkin mitophagy pathway. Based in part on recent findings from in vivo mouse models in which mitofusin-mediated mitochondrial fusion or dynamin-related protein 1-mediated mitochondrial fission was conditionally interrupted in cardiac myocytes, we propose several new concepts that may provide insight into the cardiac mitochondrial dynamism-mitophagy interactome.

引用

页码：1835 / 1849

页数：15

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