Résumé
Muscular dystrophy (MD) is a group of muscle diseases that weaken the musculoskeletal system and are characterized by progressive defects in muscle proteins and death of muscle cells. Duchenne muscular dystrophy (DMD) is the most common fatal X-linked recessive disorder in humans, caused by genetic mutations of the dystrophin gene. This chapter discusses specific pathophysiological mechanisms both in skeletal and cardiac muscles, as well as principle treatments linked to oxidative stress in DMD, which could be broadly applicable to most MD. Thus, this chapter develops the concept that oxidative stress in DMD muscle plays a key role in sustaining several of the secondary pathophysiological processes such as alterations in Ca2+ homeostasis and inflammation and emphasizes the interplay between these three pathophysiological mechanisms. In this sense, any modification of one of this signal may impact the other to trigger a vicious circle and amplifying feedback and may in part explain the poor success of therapeutic approaches aiming only at reducing oxidative stress.