Exercise intervention mitigates zebrafish age-related sarcopenia via alleviating mitochondrial dysfunction

被引:10
|
作者
Sun, Chen-Chen [1 ]
Yang, Dong [1 ]
Chen, Zhang-Lin [1 ]
Xiao, Jiang-Ling [1 ]
Xiao, Qin [1 ,2 ]
Li, Cheng-Li [1 ]
Zhou, Zuo-Qiong [1 ]
Peng, Xi-Yang [1 ]
Tang, Chang Fa [1 ]
Zheng, Lan [1 ]
机构
[1] Hunan Normal Univ, Coll Phys Educ, Key Lab Phys Fitness & Exercise Rehabil Hunan Pro, Changsha 410012, Hunan, Peoples R China
[2] Hunan First Normal Univ, Inst Phys Educ, Changsha, Peoples R China
基金
中国国家自然科学基金;
关键词
15-PGDH; AMPK; SIRT1; PGC-1; alpha; exercise; mitochondrial homeostasis; sarcopenia; SKELETAL-MUSCLE ATROPHY; PATHWAY; DISEASE; ACTIVATION; AUTOPHAGY; INJURY; MODEL; MICE; AMPK;
D O I
10.1111/febs.16637
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
Sarcopenia is a common disorder that leads to a progressive decrease in skeletal muscle function in elderly people. Exercise effectively prevents or delays the onset and progression of sarcopenia. However, the molecular mechanisms underlying how exercise intervention improves skeletal muscle atrophy remain unclear. In this study, we found that 21-month-old zebrafish had a decreased swimming ability, reduced muscle fibre cross-sectional area, unbalanced protein synthesis, and degradation, increased oxidative stress, and mitochondrial dysfunction, which suggests zebrafish are a valuable model for sarcopenia. Eight weeks of exercise intervention attenuated these pathological changes in sarcopenia zebrafish. Moreover, the effects of exercise on mitochondrial dysfunction were associated with the activation of the AMPK/SIRT1/PGC-1 alpha axis and 15-PGDH downregulation. Our results reveal potential therapeutic targets and indicators to treat age-related sarcopenia using exercise intervention.
引用
收藏
页码:1519 / 1530
页数:12
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