Reactive oxygen species in inflammation and tissue injury

Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular e...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:Antioxidants & redox signaling Ročník 20; číslo 7; s. 1126
Hlavní autori: Mittal, Manish, Siddiqui, Mohammad Rizwan, Tran, Khiem, Reddy, Sekhar P, Malik, Asrar B
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.03.2014
Predmet:
Animals
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Humans
Inflammation - metabolism
Inflammation - pathology
Neutrophils - metabolism
Neutrophils - pathology
Oxidative Stress - physiology
Reactive Oxygen Species - metabolism
ISSN:1557-7716, 1557-7716
On-line prístup:Zistit podrobnosti o prístupe
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Popis
Shrnutí:Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1557-7716
1557-7716
DOI:10.1089/ars.2012.5149