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

Antioxidants

Lin-Hua Jiang¹  Ran Ding¹  Ya-Ling Yin¹ 

[1] Department of Physiology and Pathophysiology, Sino-UK Joint Laboratory of Brain Function and Injury of Henan Province, Xinxiang Medical University, Xinxiang 453003, China;

关键词: endothelial cells;    ROS;    Ca²⁺ signaling;    TRPM2 channel;    angiogenesis;    barrier dysfunction;   

DOI  :  10.3390/antiox10050718

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown