Abstract
There is endothelial hyperpermeability in sepsis,trauma,ischaemia-reperfusion injury,acute respiratory distress syndrome and thrombosis,while an important mechanism underlying this process is increased paracellular leakage of plasma fluid and protein because of cytoskeleton contration under the role of histamine, thrombin,vascular endothelial growth factor and activated neutrophil. Structural changes initiate with agonist-receptor binding,followed by activation of intracellular signalling molecules,then phosphorylate alter the hypermeability of cell-cell adhesion. Targeting key signalling molecules that mediate endothelial-junction-cytoskeleton dissociation demonstrates a therapeutic potential to improve vascular barrier function during inflammatory injury. Key words: Endothelial cell; Microvascular permeability; Signal transduction; Sepsis
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call