Population
Dystrophin-deficient mdx mouse hearts (left atria, ventricular homogenates, and isolated ventricular myocytes)
Design
Preclinical
Authors
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Hypothesis-generating for DHPR dysfunction in dystrophic cardiomyopathy; leaves open relevance to human DMD and therapeutic targeting.
Dystrophin deficiency in mdx mice alters dihydropyridine receptors and delays L-type calcium channel inactivation, potentially contributing to calcium overload in dystrophic cardiac muscle.
Woolf et al. (2006) studied this question.
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