Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal.

Cardiovasc Res

Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Medicine, The Johns Hopkins University School of Medicine, 1830 E. Monument Street, Suite 9026, Baltimore, MD 21287, USA Department of Physiology and the Program in Cellular and Molecular Medicine, The Johns Hopkins School of Medicine, Baltimore, MD, USA

Published: April 2016

CaMKII is a serine-threonine protein kinase that is abundant in myocardium. Emergent evidence suggests that CaMKII may play an important role in promoting atrial fibrillation (AF) by targeting a diverse array of proteins involved in membrane excitability, cell survival, calcium homeostasis, matrix remodelling, inflammation, and metabolism. Furthermore, CaMKII inhibition appears to protect against AF in animal models and correct proarrhythmic, defective intracellular Ca(2+) homeostasis in fibrillating human atrial cells. This review considers current concepts and evidence from animal and human studies on the role of CaMKII in AF.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4777912PMC
http://dx.doi.org/10.1093/cvr/cvw002DOI Listing

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