title: Electrical consequences of cardiac myocyte: fibroblast coupling.
abstract: Gap junctions are channels which allow electrical signals to propagate through the heart from the sinoatrial node and through the atria, conduction system and onwards to the ventricles, and hence are essential for co-ordinated cardiac contraction. Twelve connexin (Cx) proteins make up one gap junction channel, of which there are three main subtypes in the heart; Cx40, Cx43 and Cx45. In the cardiac myocyte, gap junctions are present mainly at the intercalated discs between neighbouring myocytes, and assist in rapid electrical conduction throughout the ventricular myocardium. Fibroblasts provide the structural skeleton of the myocardium and fibroblast numbers significantly increase in heart disease. Fibroblasts also express connexins and this may facilitate heterocellular electrical coupling between myocytes and fibroblasts in the setting of cardiac disease. Interestingly, cardiac fibroblasts have been demonstrated to increase Cx43 expression in experimental models of myocardial infarction and functional gap junctions between myocytes and fibroblasts have been reported. Therefore, in the setting of heart disease enhanced cardiac myocyte: fibroblast coupling may influence the electrical activity of the myocyte and contribute to arrhythmias.
authors.affiliation: *Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
authors.forename: Lisa
authors.initials: L
authors.lastname: McArthur
authors.affiliation: *Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
authors.forename: Lisa
authors.initials: L
authors.lastname: Chilton
authors.affiliation: *Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
authors.forename: Godfrey L
authors.initials: GL
authors.lastname: Smith
authors.affiliation: *Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
authors.forename: Stuart A
authors.initials: SA
authors.lastname: Nicklin
mesh_terms: D001145:Arrhythmias, Cardiac / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D053840:Brugada Syndrome; D000075224:Cardiac Conduction System Disease; D002450:Cell Communication / Q000235:genetics; D018031:Connexin 43 / Q000096:biosynthesis* / Q000378:metabolism; D004553:Electric Conductivity; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D017629:Gap Junctions / Q000235:genetics* / Q000378:metabolism; D006329:Heart Conduction System / Q000002:abnormalities / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology
chemical_list: D018031:Connexin 43; C500216:GJA1 protein, human