Why the study?
Is CaMKII equally responsible for inducing sarcoplasmic reticulum Ca2+ leak in human ischemic and dilated cardiomyopathy?
Is CaMKII equally responsible for inducing sarcoplasmic reticulum Ca2+ leak in human ischemic and dilated cardiomyopathy?
CaMKII inhibition may be a beneficial therapeutic strategy for the majority of heart failure patients, regardless of whether the etiology is ischemic or dilated cardiomyopathy.
Supports CaMKII inhibition across HF etiologies; hypothesis-generating from animal data, pending human trials.
Functional and molecular measures of the SR Ca(2+) leak are comparable in human ICM and DCM. CaMKII is equally responsible for the induction of the 'RyR2 leakiness' in both pathologies. Thus, CaMKII inhibition as a therapeutic measure may not be restricted to patients suffering from DCM but rather may be beneficial for the majority of HF patients.
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Fischer et al. (2014) studied this question.
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