Résumé :
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Dystrophin contributes to force transmission and has a protein-scaffolding role for a variety of proteins (e.g. mechanoreceptor, nNOS, DHPR&) and is thus emerged to play an important role as components of signaling pathways acting in skeletal muscle growth and function. In the current study we test the hypothesis that dystrophin may be required for muscle adaptative response following mechanical loading (ML). We have found that in the absence of dystrophin the gain in maximal force in response to ML was reduced. Dystrophin deficiency also caused decreased cellular and molecular muscle remodeling (hypertrophy) in response to ML. Moreover, the absence of dystrophin reduced the activation of crucial intracellular signaling components including mTOR and Akt involved in the muscle adaptation to ML, possibly via myostatin, follistatin and AMPKa1. Together, our results indicate that dystrophin is a new important player in the adaptative response to muscle use, acting most likely in mechanotransduction and other muscle activity-dependent signaling pathways.
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