IMR Press / FBL / Volume 16 / Issue 5 / DOI: 10.2741/3835

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Oxidative stress and endothelial dysfunction during sepsis
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1 BakerIDI, Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC 3004, Australia
2 Department of Anesthesia and Surgical ICU, Bicetre teaching hospital, 78 rue du general Leclerc 94275 Le Kremlin Bicetre CEDEX, University Paris XI Sud. France
3 Pediatric Intensive Care Unit, Teaching Hospital Necker-Enfants Malades, 161, rue de Sevres, 75015 Paris, University Paris V, France

Academic Editors: Karen Andrews, Jaye Dusting

Front. Biosci. (Landmark Ed) 2011, 16(5), 1986–1995;
Published: 1 January 2011
(This article belongs to the Special Issue The endothelium in cardiovascular disease)

Endothelial activation and dysfunction play a key role in the pathogenesis of sepsis. During septic shock, endothelial dysfunction is involved in microcirculation impairment and organ dysfunction. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have several potentially important effects on endothelial function and are implicated in physiological regulation and disease pathophysiology. The imbalance between the production of ROS and their effective removal by non-enzymatic and enzymatic antioxidants systems could induce endothelial dysfunction with alterations of vascular tone, increases in cell adhesion properties (leukocytes and platelet adhesion), increase in vascular wall permeability and a pro-coagulant state. Increasing evidence supports the idea that the principal cause of EC dysfunction during sepsis is cell injury. ROS and RNS contribute to mitochondrial dysfunction by a range of mechanisms and induce both necrotic and apoptotic cell death. Understanding the mechanisms underlying the generation of ROS and RNS in endothelial cells and the causes of endothelial dysfunction in sepsis may help provide therapeutic strategies to tackle endothelial dysfunction and microcirculatory failure in sepsis.

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