Gap Junctions formed by Connexin 43: from Normal Function to Physiological Impact in its Change in the Cardiovascular System

Abstract

Purpose: This study highlights the role of gap junctions that allow communication between adjacent cells and in the cardiovascular system, with the most abundant isoform being connexin 43, providing the basis for intercellular communication, allowing the transfer of small molecules and the propagation of calcium waves in cardiomyocytes. This review aims to provide the main information on the role of connexin 43 in the cardiovascular system and to address the pathologies associated with its alteration. Methodology: a search was carried out in the databases of the CAPES journal portal, Scielo, Scopus, Science Direct and PubMed using keywords and selecting the articles with the inclusion and exclusion criteria to structure a work aimed at students and researchers in the areas of cell biology, biophysics and physiology. Findings: This study investigated the functional and structural anomalies of Cx43 in cardiac pathologies, highlighting that the lateralization of this protein is a recurrent event in several cardiovascular diseases, often associated with dysfunctions in the rhythms and electrical conduction of the heart. Furthermore, the role of Cx43 in mitochondria was analyzed, a recently recognized aspect that has aroused increasing interest. The results indicate that alterations in Cx43 may represent a promising therapeutic target, offering new perspectives for the development of clinical disciplines in cardiac diseases. Unique contribution to theory, practice and policy: A consolidated analysis of the demonstrated evidence suggests that gap junctions, composed of different isoforms of connections, play an essential role in the transmission of the cardiac electrical impulse. From these findings, it can be inferred that both genetic diseases and acquired pathologies are associated with modifications in the levels and subcellular distribution of connexin. Changes in the expression and positioning of these proteins can therefore trigger the worsening of pathological conditions, compromising cardiac function and enhancing the development of electrical conduction dysfunctions. In this context, connections emerge as promising targets for the development of therapeutic strategies, offering new perspectives for the treatment of a wide range of cardiac diseases.