Pulmonary endothelial barrier function

The pulmonary endothelial barrier function describes the unique ability of lung vascular endothelial cells to regulate the passage of fluids, proteins, and immune cells between blood and lung tissue, while facilitating gas exchange. This barrier is maintained by a monolayer of endothelial cells connected by adherens junctions (primarily involving VE-cadherin and catenins), and is dynamically regulated by cytoskeletal structures, ion channels, and signaling enzymes such as kinases. Disruption of this function—by inflammation, infection, or trauma—leads to pathological vascular leakage, pulmonary edema, and respiratory failure, as seen in acute respiratory distress syndrome (ARDS). Therapeutic interventions target the molecular pathways that regulate this barrier, rather than the barrier itself, through drugs that influence receptor signaling, cytoskeletal dynamics, and inflammatory mediators[1][2][3][4][5][7][8].

Other names

Endothelial barrier function in the lungpulmonary vascular endothelial barrierlung endothelial barrier

Modulation of junctional proteins (VE-cadherin, catenins) phosphorylation; Inhibition or enhancement of endothelial cell cytoskeletal dynamics (e.g., ARP2/3, actin polymerization); Modulation of signaling cascades (PKC, RhoA, Src kinases); Antagonism or activation of vascular surface receptors (S1P receptors, PAR-1); Suppression or stimulation of inflammatory mediators (TNF-α, IL-1β, VEGF)