粒体自噬
线粒体分裂
线粒体
线粒体融合
细胞生物学
生物
串扰
线粒体内膜
DNAJA3公司
内膜转移酶
品脱1
自噬
化学
线粒体膜转运蛋白
膜间隙
电压依赖性阴离子通道
外膜转位酶
细胞器
第一季
MFN2型
细菌外膜
线粒体DNA
MFN1型
遗传学
细胞凋亡
基因
物理
光学
作者
Hongxu Xian,Yih‐Cherng Liou
标识
DOI:10.1038/s41418-020-00657-z
摘要
Most cellular stress responses converge on the mitochondria. Consequently, the mitochondria must rapidly respond to maintain cellular homeostasis and physiological demands by fine-tuning a plethora of mitochondria-associated processes. The outer mitochondrial membrane (OMM) proteins are central to mediating mitochondrial dynamics, coupled with continuous fission and fusion. These OMM proteins also have vital roles in controlling mitochondrial quality and serving as mitophagic receptors for autophagosome enclosure during mitophagy. Mitochondrial fission segregates impaired mitochondria in smaller sizes from the mother mitochondria and may favor mitophagy for eliminating damaged mitochondria. Conversely, mitochondrial fusion mixes dysfunctional mitochondria with healthy ones to repair the damage by diluting the impaired components and consequently prevents mitochondrial clearance via mitophagy. Despite extensive research efforts into deciphering the interplay between fission–fusion and mitophagy, it is still not clear whether mitochondrial fission essentially precedes mitophagy. In this review, we summarize recent breakthroughs concerning OMM research, and dissect the functions of these proteins in mitophagy from their traditional roles in fission–fusion dynamics, in response to distinct context, at the intersection of the OMM platform. These insights into the OMM proteins in mechanistic researches would lead to new aspects of mitochondrial quality control and better understanding of mitochondrial homeostasis intimately tied to pathological impacts.
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