Mitochondrial quality control pathways as determinants of metabolic health

被引:99
|
作者
Held, Ntsiki M. [1 ]
Houtkooper, Riekelt H. [1 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, Lab Genet Metab Dis, NL-1105 AZ Amsterdam, Netherlands
基金
欧洲研究理事会;
关键词
fission; fusion; mitochondrial dynamics; mitochondrial quality control; mitohormesis; mitophagy; ROS; UNFOLDED PROTEIN RESPONSE; INCREASING OXIDATIVE STRESS; UBIQUITIN-PROTEASOME SYSTEM; DYNAMIN-RELATED PROTEIN; DOMINANT OPTIC ATROPHY; TAIL-ANCHORED PROTEINS; CYTOCHROME-C RELEASE; MAMMALIAN-CELLS; LIFE-SPAN; CAENORHABDITIS-ELEGANS;
D O I
10.1002/bies.201500013
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
Mitochondrial function is key for maintaining cellular health, while mitochondrial failure is associated with various pathologies, including inherited metabolic disorders and age-related diseases. In order to maintain mitochondrial quality, several pathways of mitochondrial quality control have evolved. These systems monitor mitochondrial integrity through antioxidants, DNA repair systems, and chaperones and proteases involved in the mitochondrial unfolded protein response. Additional regulation of mitochondrial function involves dynamic exchange of components through mitochondrial fusion and fission. Sustained stress induces a selective autophagy - termed mitophagy - and ultimately leads to apoptosis. Together, these systems form a network that acts on the molecular, organellar, and cellular level. In this review, we highlight how these systems are regulated in an integrated context- and time-dependent network of mitochondrial quality control that is implicated in healthy aging.
引用
收藏
页码:867 / 876
页数:10
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