Why the study?
Does ARC deletion exacerbate cardiomyopathy and myocardial infarction in response to biomechanical and ischemic stress in mice?
Population
ARC-deficient mice and specimens from failing human hearts
Comparison
Biomechanical stress and ischemia/reperfusion… vs Littermate controls
Design
Preclinical
Authors
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ARC modulation should not yet inform clinical decisions; leaves open its role as a therapeutic target in human heart failure.
Does ARC deletion exacerbate cardiomyopathy and myocardial infarction in response to biomechanical and ischemic stress in mice?
ARC is a critical antiapoptotic factor required for cardioprotection against pressure overload and ischemic stress, and its downregulation is associated with human heart failure.
Donath et al. (2006) studied this question.
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