Year: 2014
Type: review
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.
Source: Frontiers in Pharmacology
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
Awards: G2635291395, Multi-Scale Modeling of the Failing Heart for Cardiac Rysynchronization Therapy, The Virtual Physiological Rat Project, NATIONAL BIOMEDICAL COMPUTATION RESOURCE, Multi-scale Systems Model of Murine Heart Failure, G9000034035, G9000301987, Training in Multi-scale Analysis of Biological Structure and Function
OpenAlex ID: W2068401800