Reactive oxygen species and endothelial barrier components

Reactive oxygen species (ROS) and endothelial barrier components represent a critical pathological axis in vascular biology rather than a single molecular target. ROS, such as superoxide and hydrogen peroxide, are chemically reactive molecules produced by enzymes like NADPH oxidase (NOX) and the mitochondrial respiratory chain (Lum & Roebuck, 2001). The endothelial barrier is maintained by a complex network of proteins, including tight junctions (e.g., Claudin-5, Occludin) and adherens junctions (e.g., VE-cadherin), which regulate the passage of fluids and solutes across the vessel wall (Dejana et al., 2008). Under pathological conditions, excessive ROS production induces oxidative stress, which activates signaling cascades like Src kinase and RhoA, leading to the phosphorylation and redistribution of these junctional proteins (Vepa et al., 1999). This disruption results in increased vascular permeability and edema, which are hallmarks of inflammatory diseases, atherosclerosis, and acute respiratory distress syndrome (ARDS) (Drummond et al., 2011). Therapeutic strategies targeting this axis focus on neutralizing ROS with antioxidants or inhibiting ROS-generating enzymes to stabilize the barrier and preserve vascular integrity (Frey et al., 2009).

Other names

ROS-mediated endothelial dysfunctionOxidative stress-induced vascular permeabilityEndothelial junctional protein regulation by ROSROS-induced barrier disruption

Inhibition of ROS production via NADPH oxidase antagonism or direct scavenging of reactive species to prevent the oxidative modification, phosphorylation, and internalization of endothelial junction proteins such as VE-cadherin and Occludin.