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Clin Exp Pharmacol Physiol. 2010 Mar;37(3):397-401. doi: 10.1111/j.1440-1681.2009.05312.x. Epub 2009 Sep 28.

Novel role for ß-adrenergic signalling in skeletal muscle growth, development and regeneration.

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1
Basic and Clinical Myology Laboratory, Department of Physiology, The University of Melbourne, Parkville, Vic., Australia.

Abstract

1. In adult mammals, skeletal muscle mass is maintained through a precise balance of protein synthesis and protein degradation, whereas during development cellular (not protein) turnover predominates. When protein balance is shifted towards synthesis, skeletal muscle hypertrophy ensues. In contrast, increased protein degradation leads to skeletal muscle atrophy. Insulin-like growth factor (IGF)-I is among the best documented of the growth factors and regulates skeletal muscle mass by increasing protein synthesis and decreasing protein degradation. However, an IGF-I-independent growth pathway has been identified that involves the activation of beta-adrenoceptors and subsequent skeletal muscle growth, development and hypertrophy. 2. Although the importance of beta-adrenergic signalling in the heart has been well documented and continues to receive significant attention, it is only more recently that we have started to appreciate the importance of this signalling pathway in skeletal muscle structure and function. Studies have identified an important role for beta-adrenoceptors in myogenesis and work from our laboratory has identified a novel role for beta-adrenoceptors in regulating skeletal muscle regeneration after myotoxic injury. In addition, new data suggest that beta-adrenoceptors are markedly upregulated during differentiation of C2C12 cells. 3. It is now clear that beta-adrenoceptors play an important role in regulating skeletal muscle structure and function. Importantly, a clearer understanding of the pathways regulating skeletal muscle mass may lead to the identification of novel therapeutic targets for the treatment of muscle wasting disorders, including sarcopenia, cancer cachexia and the muscular dystrophies.

[Indexed for MEDLINE]

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