4.5 Review

Role of CaMKII for signaling and regulation in the heart

Journal

FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 14, Issue -, Pages 486-496

Publisher

BIOSCIENCE RESEARCH INST-BRI
DOI: 10.2741/3257

Keywords

Calcium; Calmodulin; Calcium/Calmodulin-Dependent Protein Kinase II; CaMKII; Excitation-Contraction Coupling; ECC; Excitation-Transcription Coupling; ETC; Heart; Heart Failure; hypertrophy

Funding

  1. Deutsche Forschungsgemeinschaft (DFG) [MA 1982/1-5]
  2. Heisenberg-grant [1982/3-1]
  3. DFG Klinische Forschergruppe [MA 1982/2-1]

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.5
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available