Journal
CELLULAR SIGNALLING
Volume 23, Issue 9, Pages 1441-1446Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2011.05.003
Keywords
Myostatin; Metabolism; Signal pathways; miRNAs
Categories
Funding
- National Basic Research Program of China [2004CB117506]
- National Natural Science Foundation of China [30972119]
- Sichuan Provincial Education Department [00924800]
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Myostatin, a member of the transforming growth factor-beta (TGF-beta) superfamily, is a critical autocrine/paracrine inhibitor of skeletal muscle growth. Since the first observed double-muscling phenotype was reported in myostatin-null animals, a functional role of myostatin has been demonstrated in the control of skeletal muscle development. However, beyond the confines of its traditional role in muscle growth inhibition, myostatin has recently been shown to play an important role in metabolism. During the past several years, it has been well established that Smads are canonical mediators of signals for myostatin from the receptors to the nucleus. However, growing evidence supports the notion that Non-Smad signal pathways also participate in myostatin signaling. Myostatin expression is increased in muscle atrophy and metabolic disorders, suggesting that changes in endogenous expression of myostatin may provide therapeutic benefit for these diseases. MicroRNAs (miRNAs) are a class of non-coding RNAs that negatively regulate gene expression and recent evidence has accumulated supporting a role for miRNAs in the regulation of myostatin expression. This review highlights some of these areas in myostatin research: a novel role in metabolism, signal pathways, and miRNA-mediated expression regulation. (C) 2011 Elsevier Inc. All rights reserved.
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