title: [Changes in cytosolic Ca2+dynamics associated with muscular dystrophy.]
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.
authors.affiliation: Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Japan.
authors.forename: Jun
authors.initials: J
authors.lastname: Tanihata
authors.affiliation: Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Japan.
authors.forename: Shin'ichi
authors.initials: S
authors.lastname: Takeda
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D003600:Cytosol / Q000378:metabolism*; D006801:Humans; D020388:Muscular Dystrophy, Duchenne / Q000378:metabolism*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism
chemical_list: D019837:Ryanodine Receptor Calcium Release Channel; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium