Mechanisms of CaMKII Activation in the Heart

Calcium/calmodulin (Ca(2+)/CaM) dependent protein kinase II (CaMKII) has emerged as a key nodal protein in the regulation of cardiac physiology and pathology. Due to the particularly elegant relationship between the structure and function of the kinase, CaMKII is able to translate a diverse set of s...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in pharmacology Vol. 5; p. 59
Main Author Erickson, Jeffrey R
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 02.04.2014
Subjects
Pharmacology
heart failure
CaMKII
diabetes
O-GlcNAc modification
oxidative stress
Online AccessGet full text

Cover

More Information
Summary:Calcium/calmodulin (Ca(2+)/CaM) dependent protein kinase II (CaMKII) has emerged as a key nodal protein in the regulation of cardiac physiology and pathology. Due to the particularly elegant relationship between the structure and function of the kinase, CaMKII is able to translate a diverse set of signaling events into downstream physiological effects. While CaMKII is typically autoinhibited at basal conditions, prolonged rapid Ca(2+) cycling can activate the kinase and allow post-translational modifications that depend critically on the biochemical environment of the heart. These modifications result in sustained, autonomous CaMKII activation and have been associated with pathological cardiac signaling. Indeed, improved understanding of CaMKII activation mechanisms could potentially lead to new clinical therapies for the treatment or prevention of cardiovascular disease. Here we review the known mechanisms of CaMKII activation and discuss some of the pathological signaling pathways in which they play a role.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
Reviewed by: Yanggan Wang, Zhongnan Hospital of Wuhan University, China; K. Ulrich Bayer, School of Medicine – University of Colorado Denver, USA
Edited by: Anthony W. Herren, University of California, USA
This article was submitted to Pharmacology of Ion Channels and Channelopathies, a section of the journal Frontiers in Pharmacology.
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2014.00059