Molecular and cellular mechanisms of skeletal muscle atrophy: an update

Journal of Cachexia, Sarcopenia and Muscle

Fanzani Alessandro¹  Conraads Viviane M.²  Penna Fabio³ 

[1] Department of Biomedical Sciences and Biotechnologies and Interuniversitary Institute of Myology (IIM), University of Brescia, Brescia;Antwerp University Hospital, Edegem;Department of Biochemistry and Molecular Biology, University of Barcelona, Barcelona

关键词: Skeletal muscle atrophy;    Cachexia;    Proteasome;    Autophagy;    Apoptosis;    Therapy;   

DOI  :  10.1007/s13539-012-0074-6

来源: Wiley

【 摘 要 】

Abstract

Skeletal muscle atrophy is defined as a decrease in muscle mass and it occurs when protein degradation exceeds protein synthesis. Potential triggers of muscle wasting are long-term immobilization, malnutrition, severe burns, aging as well as various serious and often chronic diseases, such as chronic heart failure, obstructive lung disease, renal failure, AIDS, sepsis, immune disorders, cancer, and dystrophies. Interestingly, a cooperation between several pathophysiological factors, including inappropriately adapted anabolic (e.g., growth hormone, insulin-like growth factor 1) and catabolic proteins (e.g., tumor necrosis factor alpha, myostatin), may tip the balance towards muscle-specific protein degradation through activation of the proteasomal and autophagic systems or the apoptotic pathway. Based on the current literature, we present an overview of the molecular and cellular mechanisms that contribute to muscle wasting. We also focus on the multifacetted therapeutic approach that is currently employed to prevent the development of muscle wasting and to counteract its progression. This approach includes adequate nutritional support, implementation of exercise training, and possible pharmacological compounds.

【 授权许可】

CC BY-NC   
© 2012 The Authors. Published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders

Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.