Caveolin-3 regulates myostatin signaling. Mini-review

Y. Ohsawa, T. Okada, A. Kuga, S. Hayashi, T. Murakami, Kunihiro Tsuchida, S. Noji, Y. Sunada

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Abstract

Caveolins, components of the uncoated invaginations of plasma membrane, regulate signal transduction and vesicular trafficking. Loss of caveolin-3, resulting from dominant negative mutations of caveolin-3 causes autosomal dominant limb-girdle muscular dystrophy (LGMD) 1C and autosomal dominant rippling muscle disease (AD-RMD). Myostatin, a member of the muscle-specific transforming growth factor (TGF)-β superfamily, negatively regulates skeletal muscle volume. Herein we review caveolin-3 suppressing of activation of type I myostatin receptor, thereby inhibiting subsequent intracellular signaling. In addition, a mouse model of LGMD1C has shown atrophic myopathy with enhanced myostatin signaling. Myostatin inhibition ameliorates muscular phenotype in the model mouse, accompanied by normalized myostatin signaling. Enhanced myostatin signaling by caveolin-3 mutation in human may contribute to the pathogenesis of LGMD1C. Therefore, myostatin inhibition therapy may be a promising treatment for patients with LGMD1C. More recent studies concerning regulation of TGF-β superfamily signaling by caveolins have provided new insights into the pathogenesis of several human diseases.

Original languageEnglish
Pages (from-to)19-24
Number of pages6
JournalActa Myologica
Volume27
Issue numberJULY
Publication statusPublished - 01-07-2008

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All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Ohsawa, Y., Okada, T., Kuga, A., Hayashi, S., Murakami, T., Tsuchida, K., Noji, S., & Sunada, Y. (2008). Caveolin-3 regulates myostatin signaling. Mini-review. Acta Myologica, 27(JULY), 19-24.