Key result
In mdx mice with dystrophic cardiomyopathy, NOX2 inhibition restored cardiomyocyte contractility and intracellular calcium handling, and reduced arrhythmogenic spontaneous calcium release.
Why the study?
Does NOX2 inhibition improve contractility and intracellular calcium handling in a mouse model of dystrophic cardiomyopathy?
Population
100 mice at 19 months of age, comprising 45 mdx mice with established dystrophic cardiomyopathy and 55…
Comparison
NOX2 inhibition using apocynin or VAS2870… vs Vehicle or untreated wild-type and mdx controls.
Design
Preclinical
Authors
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NOX2 inhibition may improve contractility in mdx cardiomyopathy; leaves open translation to human Duchenne muscular dystrophy.
Does NOX2 inhibition improve contractility and intracellular calcium handling in a mouse model of dystrophic cardiomyopathy?
In a mouse model of Duchenne muscular dystrophy, NOX2 inhibition restores cardiomyocyte contractility and normalizes sarcoplasmic reticulum calcium handling, highlighting a potential therapeutic target for dystrophic cardiomyopathy.
González et al. (2014) studied Dystrophic cardiomyopathy (n=100). NOX2 inhibition (apocynin or VAS2870) vs. Vehicle or wild-type controls was evaluated on Cardiomyocyte contractility and intracellular calcium handling. In mdx mice with dystrophic cardiomyopathy, NOX2 inhibition restored cardiomyocyte contractility and intracellular calcium handling, and reduced arrhythmogenic spontaneous calcium release.
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