Dysregulation of cell adhesion proteins and cardiac arrhythmogenesis.
Proper mechanical and electrical coupling of cardiomyocytes is crucial for normal propagation of the electrical impulse throughout the working myocardium. Various proteins on the surface of cardiomyocytes are responsible for the integration of structural information and cell-cell communication. Increasing evidence from diseased myocardium and animal models indicates that alteration in electrical coupling via gap junctions is a critical determinant in the development of an arrhythmogenic substrate. What is less clear is how gap junctions are maintained and regulated in the working myocardium. In this review, we present data from human disease and animal models that support the idea that cell adhesion proteins regulate the stability of the gap junction protein, connexin.
Li
Jifen
J
Center for Research on Reproduction and Women's Health, University of Pennsylvania, 1355 Biomedical Research Building II/III, 421 Curie Blvd., Philadelphia, Pennsylvania 19104, USA.
Patel
Vickas V
VV
Radice
Glenn L
GL
D000818:Animals; D015703:Antigens, CD / Q000502:physiology*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D015820:Cadherins / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000502:physiology*; D002450:Cell Communication / Q000502:physiology; D017630:Connexins / Q000502:physiology; D017629:Gap Junctions / Q000737:chemistry / Q000502:physiology; D006321:Heart / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D051379:Mice; D009206:Myocardium / Q000737:chemistry; D032383:Myocytes, Cardiac / Q000502:physiology; D009842:Oligopeptides / Q000502:physiology
D015703:Antigens, CD; C050361:CDH2 protein, human; D015820:Cadherins; D015815:Cell Adhesion Molecules; D017630:Connexins; D009842:Oligopeptides; C477643:rotigaptide