FIG. 3.

EC-generated ROS induce endothelial dysfunction via multiple mechanisms. In response to various agonist challenges, EC produce elevated levels of ROS that act on various signaling molecules, resulting in actin cytoskeleton remodeling and, ultimately, causing an abrupt increase in endothelial permeability. ROS-induced cytoskeletal remodeling is mediated by alterations in Ca⁺⁺ and cAMP levels, phosphorylation and redistribution of junction proteins, and phosphorylation of MLC with enhanced actomyosin contractility. On the other hand, ROS also induce the increased expression of EC adhesion molecules that leads to augmented EC inflammatory responses. cAMP, cyclic adenosine monophosphate; EC, endothelial cell.