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Cardiovascular Research 2007 73(4):631-640; doi:10.1016/j.cardiores.2006.11.005
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Copyright © 2006, European Society of Cardiology

Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation–contraction coupling in the heart

Lars S. Maier* and Donald M. Bers

Abt. Kardiologie & Pneumologie / Herzzentrum, Georg-August-Universität Göttingen, 37075 Göttingen, Germany
Department Physiology, Loyola University Chicago, Maywood, Il, USA

* Corresponding author. Abt. Kardiologie & Pneumologie / Herzzentrum, Georg-August-Universität Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany. Tel.: +49 551 39 9481 or 8921; fax: +49 551 39 8941 or 14370. Email address: lmaier{at}med.uni-goettingen.de

Calcium (Ca2+) is the central second messenger in the translation of electrical signals into mechanical activity of the heart. This highly coordinated process, termed excitation–contraction coupling or ECC, is based on Ca2+-induced Ca2+ release from the sarcoplasmic reticulum (SR). In recent years it has become increasingly clear that several Ca2+-dependent proteins contribute to the fine tuning of ECC. One of these is the Ca2+/calmodulin-dependent protein kinase (CaMK) of which CaMKII is the predominant cardiac isoform. During ECC CaMKII phosphorylates several Ca2+ handling proteins with multiple functional consequences. CaMKII may also be co-localized to distinct target proteins. CaMKII expression as well as activity are reported to be increased in heart failure and CaMKII overexpression can exert distinct and novel effects on ECC in the heart and in isolated myocytes of animals. In the present review we summarize important aspects of the role of CaMKII in ECC with an emphasis on recent novel findings.

KEYWORDS Calcium; Calmodulin; CaM kinase; E-C coupling; Heart

Time for primary review 33 days


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