Abstract
Duchenne muscular dystrophy(DMD)is X-linked genetic disorder caused by a lack of the membrane-associated protein dystrophin. DMD is characterized by progressive muscle wasting secondary to repeated muscle damage and inadequate repair. The mechanisms underlying the functional impairments in dystrophic muscle have not yet been fully determined. However, several recent studies indicate that elevated intracellular Ca2+homeostasis is a cause or facilitator of the development of muscle weakness in muscular dystrophy. This review focuses on abnormalities of Ca2+homeostasis and the possibilities for treatment by counteracting the Ca2+dysregulation.
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