Abstract
The multifunctional Ca2+/Calmodulin-dependent protein kinase II (CaMKII) is a highly validated driver of cardiac illnesses including heart failure, ischemia/reperfusion injury, and arrhythmias. Excessive CaMKII activity causes intracellular Ca2+ dysregulation, inflammation, maladaptive reprogramming, and cell death. Multiple animal studies show that CaMKII inhibition is cardioprotective in various cardiac injury models. Despite this, there are currently no approved CaMKII inhibiting therapies. Thus, development of safe and effective CaMKII inhibitors is a translational priority.
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