肌萎缩
自噬
生物
细胞生物学
骨骼肌
内分泌学
生物化学
细胞凋亡
作者
David Sebastián,Marc Beltrà,Andrea Irazoki,David Sala,Pilar Aparicio,Cecilia Aris,Esmaeil Alibakhshi,María Rubio-Valera,Manuel Palacı́n,Juan Castellanos,Luis Lores,António Zorzano
出处
期刊:Autophagy
[Informa]
日期:2024-03-28
卷期号:: 1-10
标识
DOI:10.1080/15548627.2024.2333717
摘要
Sarcopenia is a major contributor to disability in older adults, and thus, it is key to elucidate the mechanisms underlying its development. Increasing evidence suggests that impaired macroautophagy/autophagy contributes to the development of sarcopenia. However, the mechanisms leading to reduced autophagy during aging remain largely unexplored, and whether autophagy activation protects from sarcopenia has not been fully addressed. Here we show that the autophagy regulator TP53INP2/TRP53INP2 is decreased during aging in mouse and human skeletal muscle. Importantly, chronic activation of autophagy by muscle-specific overexpression of TRP53INP2 prevents sarcopenia and the decline of muscle function in mice. Acute re-expression of TRP53INP2 in aged mice also improves muscle atrophy, enhances mitophagy, and reduces ROS production. In humans, high levels of TP53INP2 in muscle are associated with increased muscle strength and healthy aging. Our findings highlight the relevance of an active muscle autophagy in the maintenance of muscle mass and prevention of sarcopenia.
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