© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Molecular mechanisms of remodeling in human atrial fibrillation
aDepartment of Radiation and Stress Cell Biology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
bDepartment of Clinical Pharmacology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
cDepartment of Cardiology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
dDepartment of Cardiology, University of Maastricht, Maastricht, The Netherlands
* Corresponding author. Tel.: +31-50-363-2911; fax: +31-50-363-2913 B.J.J.M.Brundel{at}med.rug.nl
An important acknowledgement of the last several years is that atrial fibrillation (AF) modifies the electrical properties of the atrium in a way that promotes its occurrence and maintenance. This arrhythmogenic electrophysiological remodeling is well established, but can not explain by itself that ‘AF begets AF’. This review describes molecular changes involving rapid functional alterations and slower changes in protein expression that cause electrical remodeling and contractile dysfunction in AF. An important molecular feature of AF is the reduction in L-type Ca2+ channel function and protein expression. This reduction may serve to protect the cell against a potentially lethal Ca2+ overload resulting from the increased activation rate in AF. Further, the review discusses the possible role of proteolytic systems, notably the calpains, as a mechanism linking Ca2+ overload to reduced protein expression. Thus, it appears that the elaborate molecular changes in AF are directed primarily at protecting the myocyte from cellular stress. However, such early protection occurs at the expense of electrophysiological changes that promote the long-term maintenance of AF.
KEYWORDS Ion channels; Contractile function; Arrhythmia (mechanisms)
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