Abstract
Background: Duchenne muscular dystrophy (DMD) is a severe striated muscle disease characterized by progressive muscle degeneration due to the absence of dystrophin, a cytoskeletal protein. Ninety percent of DMD patients develop cardiomyopathy. Dystrophin deficiency results in dysfunctional sodium channels and conduction abnormalities in the hearts of mdx mice, the most widely used animal model of DMD. Disease progression in the mdx mouse only modestly reflects that of DMD patients, possibly due to the upregulation of utrophin, a homologue of dystrophin.
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