Role of CaMKII for signaling and regulation in the heart

被引:39
|
作者
Maier, Lars S. [1 ]
机构
[1] Univ Gottingen, Dept Cardiol & Pneumol, Ctr Heart, D-37075 Gottingen, Germany
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷
关键词
Calcium; Calmodulin; Calcium/Calmodulin-Dependent Protein Kinase II; CaMKII; Excitation-Contraction Coupling; ECC; Excitation-Transcription Coupling; ETC; Heart; Heart Failure; hypertrophy; PROTEIN-KINASE-II; FREQUENCY-DEPENDENT ACCELERATION; SARCOPLASMIC-RETICULUM CA2+; CARDIAC RYANODINE RECEPTOR; ATRIAL-NATRIURETIC-FACTOR; RAT VENTRICULAR MYOCYTES; MEF2 TRANSCRIPTION FACTOR; OUTWARD POTASSIUM CURRENT; NUCLEAR DELTA(B) ISOFORM; CALCIUM-RELEASE CHANNEL;
D O I
10.2741/3257
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:486 / 496
页数:11
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