Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.

Front Pharmacol

Department of Bioengineering, University of California San Diego La Jolla, CA, USA ; Institute for Experimental Medicine, Oslo University Hospital Ullevål Oslo, Norway ; Simula Research Laboratory Lysaker, Norway.

Published: July 2014

AI Article Synopsis

  • CaMKII activity plays a key role in causing arrhythmias across various heart conditions, regardless of structural changes or underlying causes.
  • The involvement of CaMKII suggests that there may be a universal mechanism for arrhythmia or that different heart issues reveal distinct ways CaMKII contributes to arrhythmia.
  • This review examines existing evidence to clarify how CaMKII functions at the molecular level and its impact on arrhythmia in different heart disease scenarios.

Article Abstract

Calcium/calmodulin-dependent protein kinase II (CaMKII) activity has been shown to contribute to arrhythmogenesis in a remarkably broad range of cardiac pathologies. Several of these involve significant structural and electrophysiologic remodeling, whereas others are due to specific channelopathies, and are not typically associated with arrhythmogenic changes to protein expression or cellular and tissue structure. The ability of CaMKII to contribute to arrhythmia across such a broad range of phenotypes suggests one of two interpretations regarding the role of CaMKII in cardiac arrhythmia: (1) some CaMKII-dependent mechanism is a common driver of arrhythmia irrespective of the specific etiology of the disease, or (2) these different etiologies expose different mechanisms by which CaMKII is capable of promoting arrhythmia. In this review, we dissect the available mechanistic evidence to explore these two possibilities and discuss how the various molecular actions of CaMKII promote arrhythmia in different pathophysiologic contexts.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062880PMC
http://dx.doi.org/10.3389/fphar.2014.00110DOI Listing

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