| Literature DB >> 26499977 |
Pecoraro Michela1, Verrilli Velia1, Pinto Aldo1, Popolo Ada2.
Abstract
Gap junctions (GJs) channels provide the basis for intercellular communication in the cardiovascular system for maintenance of the normal cardiac rhythm, regulation of vascular tone and endothelial function as well as metabolic interchange between the cells. They allow the transfer of small molecules and may enable slow calcium wave spreading, transfer of "death" or of "survival" signals. In the cardiomyocytes the most abundant isoform is Connexin 43 (Cx43). Alterations in Cx43 expression and distribution were observed in myocardium disease; i.e. in hypertrophic cardiomyopathy, heart failure and ischemia. Recent reports suggest the presence of Cx43 in the mitochondria as well, at least in the inner mitochondrial membrane, where it plays a central role in ischemic preconditioning. In this review, the current knowledge on the relationship between the remodeling of cardiac gap junctions and cardiac diseases are summarized.Entities:
Keywords: AAP10; Cardiovascular disease; Connexin 43; DIAZOXIDE; GAP-134; GAP-26; GAP-27; GELDANAMYCIN; Gap junction; HEPTANOL; Mitochondria; RADICICOL; RXP-E; ZP123
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Year: 2015 PMID: 26499977 DOI: 10.1016/j.ejphar.2015.10.030
Source DB: PubMed Journal: Eur J Pharmacol ISSN: 0014-2999 Impact factor: 4.432