The importance of mitochondrial quality control for maintaining skeletal muscle function across health span

被引:32
|
作者
Sligar, James [1 ,2 ]
DeBruin, Danielle A. [3 ,4 ]
Saner, Nicholas J. [5 ]
Philp, Ashleigh M. [1 ,2 ]
Philp, Andrew [1 ,2 ]
机构
[1] Garvan Inst Med Res, Mitochondrial Metab & Ageing Lab, Sydney, NSW, Australia
[2] UNSW Sydney, UNSW Med, St Vincents Med Sch, Sydney, NSW, Australia
[3] Victoria Univ, Sunshine Hosp, Australian Inst Musculoskeletal Sci, St Albans, Vic, Australia
[4] Victoria Univ, Inst Hlth & Sport, Melbourne, Vic, Australia
[5] Baker Heart & Diabet Inst, Human Integrat Physiol, Melbourne, Vic, Australia
来源
关键词
aging; metabolism; mitochondria; sarcopenia; skeletal muscle; HIGH-INTENSITY EXERCISE; ENDOPLASMIC-RETICULUM; INDUCED MITOPHAGY; PROTEIN; AGE; BIOGENESIS; AUTOPHAGY; FISSION; FUSION; CAPACITY;
D O I
10.1152/ajpcell.00388.2021
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
As the principal energy-producing organelles of the cell, mitochondria support numerous biological processes related to metabolism, growth, and regeneration in skeletal muscle. Deterioration in skeletal muscle functional capacity with age is thought to be driven in part by a reduction in skeletal muscle oxidative capacity and reduced fatigue resistance. Underlying this maladaptive response is the development of mitochondrial dysfunction caused by alterations in mitochondrial quality control (MQC), a term encompassing processes of mitochondrial synthesis (biogenesis), remodeling (dynamics), and degradation (mitophagy). Knowledge regarding the role and regulation of MQC in skeletal muscle and the influence of aging in this process has rapidly advanced in the past decade. Given the emerging link between aging and MQC, therapeutic approaches to manipulate MQC to prevent mitochondrial dysfunction during aging hold tremendous therapeutic potential.
引用
收藏
页码:C461 / C467
页数:7
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