蛋白质水解
肌萎缩
氧化应激
自噬
蛋白酶体
合成代谢
骨骼肌
分解代谢
线粒体
细胞生物学
细胞凋亡
蛋白质降解
泛素
生物
氧化磷酸化
内分泌学
蛋白质稳态
生物化学
酶
新陈代谢
基因
作者
Lydie Combaret,Dominique Dardevet,Daniel Béchet,Daniel Taillandier,Laurent Mosoni,Didier Attaix
出处
期刊:Current Opinion in Clinical Nutrition and Metabolic Care
[Ovid Technologies (Wolters Kluwer)]
日期:2009-01-01
卷期号:12 (1): 37-41
被引量:132
标识
DOI:10.1097/mco.0b013e32831b9c31
摘要
To understand age-related changes in proteolysis and apoptosis in skeletal muscle in relation to oxidative stress and mitochondrial alterations.During aging, a progressive loss of muscle mass (sarcopenia) has been described in both human and rodents. Sarcopenia is attributable to an imbalance between protein synthesis and degradation or between apoptosis and regeneration processes or both. Major age-dependent alterations in muscle proteolysis are a lack of responsiveness of the ubiquitin-proteasome-dependent proteolytic pathway to anabolic and catabolic stimuli and alterations in the regulation of autophagy. In addition, increased oxidative stress leads to the accumulation of damaged proteins, which are not properly eliminated, aggregate, and in turn impair proteolytic activities. Finally, the mitochondria-associated apoptotic pathway may be activated. These age-induced changes may contribute to sarcopenia and decreased ability of old individuals to recover from stress.Alterations in proteasome-dependent or lysosomal proteolysis, increased oxidative stress, mitochondrial dysfunction, and apoptosis presumably contribute to the development of sarcopenia.
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