Cellular and molecular mechanisms of muscle atrophy

被引:957
作者
Bonaldo, Paolo [1 ]
Sandri, Marco [1 ,2 ]
机构
[1] Univ Padua, Dept Biomed Sci, I-35131 Padua, Italy
[2] Venetian Inst Mol Med, Dulbecco Telethon Inst, I-35129 Padua, Italy
关键词
FOXO TRANSCRIPTION FACTORS; RETRACTED ARTICLE. SEE; ADULT SKELETAL-MUSCLE; GROWTH-FACTOR-I; RING FINGER 1; UBIQUITIN LIGASES; PROTEIN-DEGRADATION; MYOBLAST DIFFERENTIATION; TRANSGENIC MICE; GLUCOCORTICOID-RECEPTOR;
D O I
10.1242/dmm.010389
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Skeletal muscle is a plastic organ that is maintained by multiple pathways regulating cell and protein turnover. During muscle atrophy, proteolytic systems are activated, and contractile proteins and organelles are removed, resulting in the shrinkage of muscle fibers. Excessive loss of muscle mass is associated with poor prognosis in several diseases, including myopathies and muscular dystrophies, as well as in systemic disorders such as cancer, diabetes, sepsis and heart failure. Muscle loss also occurs during aging. In this paper, we review the key mechanisms that regulate the turnover of contractile proteins and organelles in muscle tissue, and discuss how impairments in these mechanisms can contribute to muscle atrophy. We also discuss how protein synthesis and degradation are coordinately regulated by signaling pathways that are influenced by mechanical stress, physical activity, and the availability of nutrients and growth factors. Understanding how these pathways regulate muscle mass will provide new therapeutic targets for the prevention and treatment of muscle atrophy in metabolic and neuromuscular diseases.
引用
收藏
页码:25 / 39
页数:15
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