IMR Press / FBL / Volume 14 / Issue 2 / DOI: 10.2741/3257

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Role of CaMKII for signaling and regulation in the heart
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1 Department of Cardiology and Pneumology, Heart Center, Georg-August-University Goettingen, Robert-Koch-Strasse 40, 37075 Goettingen, Germany
Front. Biosci. (Landmark Ed) 2009, 14(2), 486–496; https://doi.org/10.2741/3257
Published: 1 January 2009
Abstract

The Ca2+/calmodulin-dependent protein kinase II (CaMKII) is the CaMK isoform predominantly found in the heart. Cardiac myocytes signaling during excitation-contraction coupling (ECC) is described by the increase in intracellular Ca2+ concentration. In consequence, CaMKII is activated thereby phosphorylating several important Ca2+ handling proteins with multiple functional consequences for cardiac myocytes. Specific CaMKII overexpression in the heart and in isolated myocytes of animals can exert distinct and novel effects on ECC. CaMKII activity and expression are reported to be increased in cardiac hypertrophy, in human heart failure, as well as in animal models thereby contributing to cardiac disease through a regulation process termed excitation-transcription coupling (ETC). In the present review important aspects of the role of CaMKII in ECC and ETC are summarized with an emphasis on recent novel findings.

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