Experimental Antiarrhythmic Targets: CaMKII Inhibition – Ready for Clinical Evaluation?

Author(s): Lars S. Maier

Journal Name: Current Medicinal Chemistry

Volume 21 , Issue 11 , 2014

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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+ leak.

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Article Details

Year: 2014
Published on: 26 June, 2013
Page: [1299 - 1307]
Pages: 9
DOI: 10.2174/09298673113209990171
Price: $65

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