Key result
CaMKII inhibition acutely improved contractility in human failing myocardium by reducing sarcoplasmic reticulum Ca2+ leak and increasing Ca2+ load.
Why the study?
Does CaMKII inhibition improve contractility in end-stage failing human myocardium?
Does CaMKII inhibition improve contractility in end-stage failing human myocardium?
CaMKII inhibition acutely improves contractility in human failing myocardium by reducing SR Ca2+ leak, suggesting a potential therapeutic target for heart failure.
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Identifies CaMKII as HF drug target; leaves open clinical translation from ex vivo data.
Sossalla et al. (2010) studied Heart failure (dilated and ischemic cardiomyopathy). CaMKII inhibitors (KN-93 and AIP) vs. Untreated / nonfailing myocardium was evaluated on Contractility (force frequency relationships and postrest twitches). CaMKII inhibition acutely improved contractility in human failing myocardium by reducing sarcoplasmic reticulum Ca2+ leak and increasing Ca2+ load.