粒体自噬
线粒体
线粒体生物发生
骨骼肌
细胞器
自噬
细胞生物学
细胞器生物发生
生物
医学
内科学
内分泌学
生物发生
生物化学
细胞凋亡
基因
作者
David A. Hood,Jonathan M. Memme,Ashley N. Oliveira,Matthew Triolo
出处
期刊:Annual Review of Physiology
[Annual Reviews]
日期:2018-09-16
卷期号:81 (1): 19-41
被引量:363
标识
DOI:10.1146/annurev-physiol-020518-114310
摘要
Mitochondria are critical organelles responsible for regulating the metabolic status of skeletal muscle. These organelles exhibit remarkable plasticity by adapting their volume, structure, and function in response to chronic exercise, disuse, aging, and disease. A single bout of exercise initiates signaling to provoke increases in mitochondrial biogenesis, balanced by the onset of organelle turnover carried out by the mitophagy pathway. This accelerated turnover ensures the presence of a high functioning network of mitochondria designed for optimal ATP supply, with the consequence of favoring lipid metabolism, maintaining muscle mass, and reducing apoptotic susceptibility over the longer term. Conversely, aging and disuse are associated with reductions in muscle mass that are in part attributable to dysregulation of the mitochondrial network and impaired mitochondrial function. Therefore, exercise represents a viable, nonpharmaceutical therapy with the potential to reverse and enhance the impaired mitochondrial function observed with aging and chronic muscle disuse.
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