title: Regulation of endothelial barrier function by reactive oxygen and nitrogen species.
abstract: Excessive generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), by activated neutrophils and endothelial cells, has been implicated in the pathophysiology of endothelial barrier dysfunction. Disruption of the integrity of this barrier markedly increases permeability to fluids, solutes and inflammatory cells and is the hallmark of many disorders such as acute lung injury (ALI) and sepsis. There has been considerable progress in our understanding of the sequence of molecular and structural events that mediate the response of endothelial cells to oxidants and nitrosants. In addition, substantial experimental evidence demonstrates improvement of endothelial barrier dysfunction with antioxidant strategies. However, no significant benefits have been observed, so far, in clinical trials of antioxidants for the treatment of endothelial barrier dysfunction. This article will review the available evidence implicating ROS and RNS in endothelial barrier dysfunction, explore potential underlying mechanisms, and identify areas of further research.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, School of Medicine, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA.
authors.forename: Adel
authors.initials: A
authors.lastname: Boueiz
authors.forename: Paul M
authors.initials: PM
authors.lastname: Hassoun
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000502:physiology*; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008171:Lung Diseases / Q000188:drug therapy; D008954:Models, Biological; D018384:Oxidative Stress / Q000502:physiology; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
chemical_list: D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species