Duchenne muscular dystrophy (DMD) is a lethal muscle degenerative disease affecting 1: 3500 male births [1]. It is caused by genetic mutations resulting in dystrophin protein deficiency. Dystrophin maintains membrane integrity; its deficiency causes myofiber damage under mechanical loading [1]. The resulting DMD muscle membrane tears impact its permeability which increases calcium concentration inside the cell and promotes inflammatory reactions and muscle degeneration [2]. Eventually, DMD muscle suffers a loss of mass, and becomes less functional due to inflammation and fibrosis [3]. Current therapies aim to slow disease progression, promote muscle regeneration and growth, and maintain muscle mass [2].