Journal
FEBS LETTERS
Volume 583, Issue 22, Pages 3600-3604Publisher
WILEY
DOI: 10.1016/j.febslet.2009.10.033
Keywords
Eccentric contraction; Calcium; TRPV2; Duchenne muscular dystrophy
Funding
- Association francaise contre les myopathies (AFM)
- Association belge contre les maladies neuro-musculaires (ABMM)
- General Direction of Scientific Research of the French Community of Belgium [ARC 05/10-328]
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Duchenne myopathy is a lethal disease due to the absence of dystrophin, a cytoskeletal protein. Muscles from dystrophin-deficient mice (mdx) typically present an exaggerated susceptibility to eccentric work characterized by an important force drop and an increased membrane permeability consecutive to repeated lengthening contractions. The present study shows that mdx muscles are largely protected from eccentric work-induced damage by overexpressing a dominant negative mutant of TRPV2 ion channel. This observation points out the role of TRPV2 channel in the physiopathology of Duchenne muscular dystrophy. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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