Mitochondrial quality control: from molecule to organelle

被引:107
作者
Roca-Portoles, Alba [1 ,2 ]
Tait, Stephen W. G. [1 ]
机构
[1] Univ Glasgow, Inst Canc Sci, Canc Res UK Beatson Inst, Switchback Rd, Glasgow G61 1BD, Lanark, Scotland
[2] Ctr Biol Mol Severo Ochoa CBMSO, Nicolas Cabrera 1, Madrid 28049, Spain
关键词
Mitochondrial dysfunction; UPRmt; ISR; Mitochondrial fission; Mitochondrial fusion; Mitophagy; PINK1; Parkin; Mitochondrial diseases; INTEGRATED STRESS-RESPONSE; UNFOLDED PROTEIN RESPONSE; DYNAMIN-RELATED PROTEIN; CELL-CYCLE; FUNCTIONAL IMPAIRMENT; TRANSLATIONAL CONTROL; PROTEOLYTIC CLEAVAGE; DISEASE IMPLICATIONS; HUNTINGTONS-DISEASE; DNA DELETIONS;
D O I
10.1007/s00018-021-03775-0
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
Mitochondria are organelles central to myriad cellular processes. To maintain mitochondrial health, various processes co-operate at both the molecular and organelle level. At the molecular level, mitochondria can sense imbalances in their homeostasis and adapt to these by signaling to the nucleus. This mito-nuclear communication leads to the expression of nuclear stress response genes. Upon external stimuli, mitochondria can also alter their morphology accordingly, by inducing fission or fusion. In an extreme situation, mitochondria are degraded by mitophagy. Adequate function and regulation of these mitochondrial quality control pathways are crucial for cellular homeostasis. As we discuss, alterations in these processes have been linked to several pathologies including neurodegenerative diseases and cancer.
引用
收藏
页码:3853 / 3866
页数:14
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