Waste not, want not: Role for caveolin-3 in muscular dystrophy

The muscular dystrophies are a group of genetic and hereditary diseases in which patients experience skeletal muscle weakness due to wasting and loss of muscle fibers. However, the signaling pathways involved in muscle wasting have remained elusive. Researchers have begun to focus on the potential role of proteins known as caveolins in muscle wasting. Caveolins come together to form a scaffold onto which many other types of signaling molecules can assemble at the cell plasma membrane. Caveolin-3 is a muscle-specific form of caveolins.

In a study appearing online on October 12, in advance of publication in the November print issue of the Journal of Clinical Investigation, Yoshihide Sunada and colleagues from Kawasaki Medical School, Japan, show that loss of caveolin-3 in a mouse model of muscular dystrophy increases the intracellular activity of myostatin – a known inhibitor of muscle growth – and leads to muscle wasting. Conversely, the authors demonstrated that inhibition of myostatin rescued the muscle wasting in these mice. The study indicates that overactivation of myostatin signaling plays an important role in the pathogenesis of muscular dystrophy in mice, and that a principal function of caveolin-3 in skeletal muscle is to inhibit myostatin signaling, thereby preventing muscle wasting. Future studies may show that myostatin inhibition may have potential as a promising therapy for patients with certain kinds of muscular dystrophy.

###

TITLE: Muscular atrophy of caveolin-3–deficient mice is rescued by myostatin inhibition

AUTHOR CONTACT:

Yoshihide Sunada

Kawasaki Medical School, Kurashiki, Japan.

Phone: 81-86-462-1111; Fax: 81-86-462-1199; E-mail: ysunada@med.kawasaki-m.ac.jp.

View the PDF of this article at: https://www.the-jci.org/article.php?id=28520


Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
    Published on PsychCentral.com. All rights reserved.

 

 

Never grow a wishbone, daughter, where your backbone ought to be.
-- Clementine Paddelford