Caveolin-3 regulates myostatin signaling. Mini-review

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

研究成果: Article査読

15 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)19-24
ページ数6
ジャーナルActa Myologica
27
JULY
出版ステータスPublished - 01-07-2008

All Science Journal Classification (ASJC) codes

  • 循環器および心血管医学

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