Experimental Antiarrhythmic Targets: CaMKII Inhibition – Ready for Clinical Evaluation?
Lars S. Maier
Affiliation: Abt. Kardiologie und Pneumologie / Herzzentrum, Deutsches Zentrum fur Herzkreislaufforschung, Georg-August-Universitat Gottingen, Robert-Koch-Str. 40 37075 Gottingen, Germany.
In the recent years, Ca2+/calmodulin-dependent protein kinase II (CaMKII) was suggested to be associated with
cardiac hypertrophy and heart failure but also with arrhythmias both in animal models as well as in the human heart. This
article focuses on the role of CaMKII for excitation-contraction coupling but more explicitly it highlights major CaMKIIdependent
proarrhythmogenic mechanisms including SR Ca2+ leak and late Na+ current. Because a clinical significance of
CaMKII is implied for both mechanisms, CaMKII inhibition is suggested to be a therapeutical approach in the near future.
Keywords: Arrhythmia, atrial fibrillation, Ca2+/calmodulin (Ca2+/CaM), Ca2+/CaM-dependent protein kinase II (CaMKII), excitation-
contraction coupling (ECC), heart failure, hypertrophy, late Na+ current (INa, late), sarcoplasmic reticulum (SR), SR Ca2+
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