Rho and Reactive Oxygen Species at Crossroads of Endothelial Permeability and Inflammation

摘要

Significance: Increased endothelial permeability and inflammation are two major hallmarks of the life-threatening conditions such as acute respiratory distress syndrome and sepsis. There is a growing consensus in the field that the Rho family of small guanosine triphosphates are critical regulators of endothelial function at both physiological and pathological states. A basal level of reactive oxygen species (ROS) is essential for maintaining metabolic homeostasis, vascular tone, and angiogenesis; however, excessive ROS generation impairs endothelial function and promotes lung inflammation. In this review, we will focus on the role of Rho in control of endothelial function and also briefly discuss a nexus between ROS generation and Rho activation during endothelial dysfunction.