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Journal of Cachexia, Sarcopenia and Muscle

Erschienen in:

01.09.2012 | Review

Molecular and cellular mechanisms of skeletal muscle atrophy: an update

verfasst von: Alessandro Fanzani, Viviane M. Conraads, Fabio Penna, Wim Martinet

Erschienen in: Journal of Cachexia, Sarcopenia and Muscle | Ausgabe 3/2012

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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.

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Titel: Molecular and cellular mechanisms of skeletal muscle atrophy: an update
verfasst von: Alessandro Fanzani
Viviane M. Conraads
Fabio Penna
Wim Martinet
Publikationsdatum: 01.09.2012
Verlag: Springer-Verlag
Erschienen in: Journal of Cachexia, Sarcopenia and Muscle / Ausgabe 3/2012
Print ISSN: 2190-5991
Elektronische ISSN: 2190-6009
DOI: https://doi.org/10.1007/s13539-012-0074-6

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