Open AccessReduced Cx43 Expression Triggers Increased Fibrosis Due to Enhanced Fibroblast Activity
Author(s) -
John A. Jansen,
Toon A.B. van Veen,
Sanne de Jong,
Roel van der Nagel,
Leonie van Stuijvenberg,
Helen E. Driessen,
Ronald p Labzowski,
Carolin M. Oefner,
Astrid A. T. M. Bosch,
Tri Q. Nguyen,
Roel Goldschmeding,
Marc A. Vos,
Jacques M.T. de Bakker,
Harold V.M. van Rijen
Publication year - 2012
Publication title -
circulation arrhythmia and electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.684
H-Index - 102
eISSN - 1941-3149
pISSN - 1941-3084
DOI - 10.1161/circep.111.966580
Subject(s) - medicine , fibrosis , cardiac fibrosis , endocrinology , pathophysiology , myocardial fibrosis , gap junction , pathology , chemistry , intracellular , biochemistry
Arrhythmogenic ventricular remodeling is hallmarked by both reduced gap junction expression and increased collagen deposition. We hypothesized that reduced connexin43 (Cx43) expression is responsible for enhanced fibrosis in the remodeled heart, resulting in an arrhythmogenic substrate. Therefore, we investigated the effect of normal or reduced Cx43 expression on the formation of fibrosis in a physiological (aging) and pathophysiological (transverse aortic constriction [TAC]) mouse model.
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