Oxidative Stress and Microvessel Barrier Dysfunction
Abstract
Clinical and experimental evidence indicate that increased vascular permeability contributes to many disease-associated vascular complications. Oxidative stress with increased production of reactive oxygen species (ROS) has been implicated in a wide variety of pathological conditions, including inflammation and many cardiovascular diseases. It is thus important to identify the role of ROS and their mechanistic significance in microvessel barrier dysfunction under pathological conditions. The role of specific ROS and their cross talk in pathological processes is complex. The mechanisms of ROS-induced increases in vascular permeability remain poorly understood. The sources of ROS in diseases have been extensively reviewed at enzyme levels. This review will instead focus on the underlying mechanisms of ROS release by leukocytes, the differentiate effects and signaling mechanisms of individual ROS on endothelial cells, pericytes and microvessel barrier function, as well as the interplay of reactive oxygen species, nitric oxide, and nitrogen species in ROS-mediated vascular barrier dysfunction. As a counter balance of excessive ROS, nuclear factor erythroid 2 related factor 2 (Nrf2), a redox-sensitive cell-protective transcription f...Continue Reading
References
Histamine increases venular permeability via a phospholipase C-NO synthase-guanylate cyclase cascade
Effects of inhaled NO and inhibition of endogenous NO synthesis in oxidant-induced acute lung injury
Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions
Serum cytokine levels in human septic shock. Relation to multiple-system organ failure and mortality
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