Autophagy in skeletal muscle

被引：368

作者：

Sandri, Marco ^{[1
]}

机构：

[1] Univ Padua, Dept Biomed Sci, Dulbecco Telethon Inst, VIMM, I-35129 Padua, Italy

来源：

FEBS LETTERS | 2010年 / 584卷 / 07期

关键词：

Autophagy; Skeletal muscle; Atrophy; Protein degradation; Muscle wasting; Akt; PROTEIN-DEGRADATION; PROTEASOME PATHWAY; ATROPHY INVOLVE; IN-VIVO; GROWTH; TRANSCRIPTION; DENERVATION; UBIQUITIN; DISEASE; FOXO3;

D O I：

10.1016/j.febslet.2010.01.056

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：

Muscle mass represents 40-50% of the human body and, in mammals, is one of the most important sites for the control of metabolism. Moreover, during catabolic conditions, muscle proteins are mobilized to sustain gluconeogenesis in the liver and to provide alternative energy substrates for organs. However, excessive protein degradation in the skeletal muscle is detrimental for the economy of the body and it can lead to death. The ubiquitin-proteasome and autophagy-lysosome systems are the major proteolytic pathways of the cell and are coordinately activated in atrophying muscles. However, the role and regulation of the autophagic pathway in skeletal muscle is still largely unknown. This review will focus on autophagy and discuss its beneficial or detrimental role for the maintenance of muscle mass. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：1411 / 1416

页数：6

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