Novel mechanisms for maintaining endothelial barrier function in sepsis.

The pathophysiology of multiple disease states, including sepsis,1,2 hypertension,1 atherosclerosis,3–5 and ischemiareperfusion injury,6 is characterized by loss of the endothelial barrier function leading to the accumulation of plasma-borne proteins, tissue edema, and cell death. Importantly therapeutic strategies that inhibit loss of endothelial barrier function have been associated with strategies that improve outcomes.7 There is growing understanding of the role of adherens in maintaining the integrity of the endothelial barrier function8 and the molecular pathways that regulate adheren expression.9