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European Heart Journal 2004 25(22):1979-1989; doi:10.1016/j.ehj.2004.08.007
Copyright © 2004 by the European Society of Cardiology.
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Review

Regulation of myocardial connexins during hypertrophic remodelling

Birgit E.J. Teunissen, Habo J. Jongsma and Marti F.A. Bierhuizen*

Department of Medical Physiology, University Medical Center Utrecht, P.O. Box 85060, 3508 AB Utrecht, The Netherlands

Received March 31, 2004; revised July 1, 2004; accepted August 5, 2004 * Corresponding author. Tel.: +31 30 253 8418; fax: +31 30 253 9036 (E-mail: m.f.a.bierhuizen{at}med.uu.nl).

Cardiac hypertrophic remodelling, initiated by signalling cascades in response to increased workload, injury or intrinsic disease, is initially adaptive. However, prolonged hypertrophy as a consequence of pathological stress leads to maladaptive changes that increase the risk for fatal ventricular arrhythmias. One of these changes is the remodelling of myocardial gap junctions, which provide for electrical coupling of adjacent cardiomyocytes. Myocardial gap junctions are composed of three connexin isotypes, connexin40 (Cx40), -43 (Cx43), and -45 (Cx45) and each display a characteristic developmental and regional expression pattern. Alterations in the distribution and expression of Cx43, the predominant isoform in the adult ventricles, has been the main focus of examination in humans, experimental animal models and cultured cardiomyocytes in response to hypertrophy. The molecular mechanisms and signalling pathways underlying these changes have been studied less thoroughly. In this review we summarize what is known about the remodelling of myocardial gap junctions during hypertrophy, the putative underlying mechanisms and functional consequences thereof.


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