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FEBS Lett. 2009 Nov 19;583(22):3600-4. doi: 10.1016/j.febslet.2009.10.033. Epub 2009 Oct 17.

Essential role of TRPV2 ion channel in the sensitivity of dystrophic muscle to eccentric contractions.

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Laboratory of Cell Physiology, Institute of Neurosciences, Université catholique de Louvain, 55/40 av Hippocrate, 1200 Brussels, Belgium.


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.

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