Targeting versican as a therapeutic strategy in Duchenne muscular dystrophy

Fibrosis drives muscle degeneration and weakness in Duchenne muscular dystrophy. This thesis identified versican as an important fibrosis-associated protein overexpressed in dystrophic muscles, with cellular expression reduced by glucocorticoids. Using novel mouse models, the importance of versican reduction in improving the contractile function of dystrophic muscles was also established.