Duchenne muscular dystrophy is a severe degenerative disorder of skeletal muscle due to the loss of dystrophin, a cytoskeletal protein associated with the inner cellular membrane of muscle fibres. The absence of dystrophin induces an abnormal influx of calcium through cationic channels in dystrophic muscle fibres. We previously showed that these channels belong to the Transient Receptor Potential (TRP) family and were activated by membrane stretch (SAC: Stretch Activated Channel). 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 investigates the possible implication of TRPV2, one of the principal candidates for the abnormally regulated Ca²⁺-entry pathway in mdx fibres. We show that the abnormal influx of Ca²⁺ is reduced in muscle fibres from mdx mice overexpressing a dominant negative mutant of TRPV2 ion channel. Interestingly, dystrophic muscles are also largely protected from eccentric work-induced damage. These observations point out the role of TRPV2 channel in the physiopathology of Duchenne muscular dystrophy.