Reactive Oxygen Species-Induced TRPM2-Mediated Ca2+ Signalling in Endothelial Cells

Endothelial cells form the innermost layer of blood vessels with a fundamental role as the physical barrier. While regulation of endothelial cell function by reactive oxygen species (ROS) is critical in physiological processes such as angiogenesis, endothelial function is a major target for interruption by oxidative stress resulting from generation of high levels of ROS in endothelial cells by various pathological factors and also release of ROS by neutrophils. TRPM2 is a ROS-sensitive Ca2+-permeable channel expressed in endothelial cells of various vascular beds. In this review, we provide an overview of the TRPM2 channel and its role in mediating ROS-induced Ca2+ signaling in endothelial cells. We discuss the TRPM2-mediated Ca2+ signaling in vascular endothelial growth factor-induced angiogenesis and in post-ischemic neovascularization. In particular, we examine the accumulative evidence that supports the role of TRPM2-mediated Ca2+ signaling in endothelial cell dysfunction caused by various oxidative stress-inducing factors that are associated with tissue inflammation, obesity and diabetes, as well as air pollution. These findings provide new, mechanistic insights into ROS-mediated regulation of endothelial cells in physiology and diseases.

Automated summary

The article discusses the importance of endothelial cell function in physiological and pathological processes, with a focus on the role of the TRPM2 channel in mediating ROS-induced calcium signaling in endothelial cells.