Open AccessImpact of Connexins on Atherogenesis: A Brief Review
Author(s) -
Veronika A. Myasoedova,
Dongwei Zhang,
Reinhard Wetzker,
Andrey V. Grechko,
Alexander N. Orekhov
Publication year - 2020
Publication title -
journal of integrative medicine
Language(s) - English
Resource type - Journals
ISSN - 2315-4616
DOI - 10.30564/jim.v7i2.184
Subject(s) - gap junction , connexin , connexon , microbiology and biotechnology , intracellular , cell signaling , cell type , homeostasis , biology , extracellular , cell , chemistry , medicine , signal transduction , biochemistry
Connexins family in humans consists of 21 highly conserved proteins that are responsible for contact formation between cells. On the cell surface, connexins form hemichannels, or connexons. Two hemichannels brought together form a gap junction, a form of intercellular contact that allows for direct transfer of material and signals between the adjacent cells. Gap junctions serve for transporting ions and other soluble, low molecular weight molecules therefore synchronizing the microenvironment of the contacting cells and maintaining cell and tissue homeostasis. Impairment of gap junctions is associated with different pathological conditions. Importantly, it has been described in atherosclerosis, which causes local cellular dysfunction in the arterial wall tissues followed by the development of atherosclerotic plaque. There are 3 main connexins expressed in human cardiovascular system: Cx37, Cx40, and Cx43. Alterations in the arterial wall cells observed in atherosclerosis include changes in the expression pattern of the main connexins and impairment of intercellular contacts and communication. According to the currently available data, Cx37 and Cx40 have anti-atherogenic and vasculoprotective properties, while Cx43 appears to be more pro-atherogenic. However, the effects of connexins are cell type-dependent and in many cases, remain to be studied in detail. In this review, we summarize the available knowledge on connexins of the arterial wall cells involved in atherosclerosis development.