Population
Cardiac ventricular myocytes enzymatically isolated from 5- to 9-month-old dystrophic mdx and wild-type mice
Comparison
Mechanical stress applied as osmotic shock vs Wild-type (WT) cardiomyocytes
Design
Preclinical
Authors
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Mechanical stress may drive Ca2+-ROS-mitochondrial damage in dystrophic cardiomyocytes; leaves open whether targeting this axis modifies cardiomyopathy progression.
In dystrophic mdx cardiomyocytes, mechanical stress triggers excessive intracellular Ca2+ signals and ROS generation, linking initial sarcolemmal injury to mitochondrial dysfunction.
Jung et al. (2007) studied this question.
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