骨骼肌
粒体自噬
线粒体生物发生
线粒体
细胞生物学
生物
再生(生物学)
肌萎缩
细胞器
氧化应激
生物发生
神经科学
内分泌学
遗传学
自噬
基因
细胞凋亡
作者
James Sligar,Danielle A Debruin,Nicholas J. Saner,Ashleigh M. Philp,Andrew Philp
出处
期刊:American Journal of Physiology-cell Physiology
[American Physiological Society]
日期:2022-03-01
卷期号:322 (3): C461-C467
被引量:14
标识
DOI:10.1152/ajpcell.00388.2021
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.
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