CaMKII as a target for arrhythmia suppression

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Abstract

Calcium/calmodulin-dependent protein kinase II (CaMKII) has emerged as key enzyme in many cardiac pathologies, especially heart failure (HF), myocardial infarction and cardiomyopathies, thus leading to contractile dysfunction and malignant arrhythmias. While many pathways leading to CaMKII activation have been elucidated in recent years, hardly any clinically viable compounds affecting CaMKII activity have progressed from basic in vitro science to in vivo studies.

This review focuses on recent advances in anti-arrhythmic strategies involving CaMKII.

Specifically, both inhibition of CaMKII itself to prevent arrhythmias, as well as anti-arrhythmic approaches affecting CaMKII activity via alterations in signaling cascades upstream and downstream of CaMKII will be discussed.

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