Mitochondrial division, fusion and degradation

被引:59
|
作者
Murata, Daisuke [1 ]
Arai, Kenta [1 ]
Iijima, Miho [1 ]
Sesaki, Hiromi [1 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Cell Biol, 725 N Wolfe St, Baltimore, MD 21205 USA
来源
JOURNAL OF BIOCHEMISTRY | 2020年 / 167卷 / 03期
基金
美国国家卫生研究院;
关键词
actin; dynamin-related GTPase; ER-mitochondria contact; lipids; mitophagy; ENDOPLASMIC-RETICULUM; MITOFUSIN; 2; PATERNAL MITOCHONDRIA; PARKINSONS-DISEASE; PHOSPHATIDIC-ACID; OPTIC ATROPHY; REQUIRES DRP1; FISSION; AUTOPHAGY; DYNAMICS;
D O I
10.1093/jb/mvz106
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
The mitochondrion is an essential organelle for a wide range of cellular processes, including energy production, metabolism, signal transduction and cell death. To execute these functions, mitochondria regulate their size, number, morphology and distribution in cells via mitochondrial division and fusion. In addition, mitochondrial division and fusion control the autophagic degradation of dysfunctional mitochondria to maintain a healthy population. Defects in these dynamic membrane processes are linked to many human diseases that include metabolic syndrome, myopathy and neurodegenerative disorders. In the last several years, our fundamental understanding of mitochondrial fusion, division and degradation has been significantly advanced by high resolution structural analyses, protein-lipid biochemistry, super resolution microscopy and in vivo analyses using animal models. Here, we summarize and discuss this exciting recent progress in the mechanism and function of mitochondrial division and fusion.
引用
收藏
页码:233 / 241
页数:9
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