Endothelial connexin-integrin crosstalk in vascular inflammation

Cardiovascular diseases including blood vessel disorders represent a major cause of death globally. The essential roles played by local and systemic vascular inflammation in the pathogenesis of cardiovascular diseases have been increasingly recognized. Vascular inflammation triggers the aberrant activation of endothelial cells, which leads to the functional and structural abnormalities in vascular vessels. In addition to humoral mediators such as pro-inflammatory cytokines and prostaglandins, the alteration of physical and mechanical microenvironment including vascular stiffness and shear stress - modify the gene expression profiles and metabolic profiles of endothelial cells via mechano-transduction pathways, thereby contributing to the pathogenesis of vessel disorders. Notably, connexins and integrins crosstalk each other in response to the mechanical stress, and, thereby, play an important role in regulating the mechano-transduction of endothelial cells. Here, we provide an overview on how the inter-play between connexins and integrins in endothelial cells unfold during the mechanotransduction in vascular inflammation.

Automated summary

Vascular inflammation plays a crucial role in the pathogenesis of cardiovascular diseases, triggering aberrant activation of endothelial cells and leading to structural and functional abnormalities in blood vessels. In addition to humoral mediators, alterations in the physical and mechanical microenvironment can modify gene expression and metabolic profiles of endothelial cells via mechano-transduction pathways, contributing to the development of vessel disorders.