Reactive oxygen species in inflammation and tissue injury.
Journal: 2014/October - Antioxidants and Redox Signaling
ISSN: 1557-7716
Abstract:
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.
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Antioxid Redox Signal 20(7): 1126-1167

Reactive Oxygen Species in Inflammation and Tissue Injury

Department of Pharmacology, Center for Lung and Vascular Biology, University of Illinois, College of Medicine, Chicago, Illinois.
Department of Pediatrics, University of Illinois at Chicago, Chicago, Illinois.
Corresponding author.
Reviewing Editors: Jerzy Beltowski, Dylan Burger, Donna Cioffi, Gábor Csányi, Andreas Daiber, Rodrigo Franco, Paul Hyslop, Thomas Kietzmann, Colin Murdoch, Vickram Ramkumar, and Thomas Resta
Address correspondence to:, Dr. Asrar B. Malik, Department of Pharmacology,, Center for Lung and Vascular Biology, University of Illinois College of Medicine, 835 S Wolcott Ave., Chicago, IL 60612, E-mail:ude.ciu@kilamba
Address correspondence to:, Dr. Asrar B. Malik, Department of Pharmacology,, Center for Lung and Vascular Biology, University of Illinois College of Medicine, 835 S Wolcott Ave., Chicago, IL 60612, E-mail:ude.ciu@kilamba
Received 2012 Dec 12; Revised 2013 Aug 19; Accepted 2013 Sep 1.

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. Antioxid. Redox Signal. 20, 1126–1167.

Abstract

Abbreviations Used

4-HNE4-hydroxy-2-nonenal
ADMAasymmetrical dimethyl arginines
AIFapoptosis-inducing factor
AJAdherens junction
Ang IIangiotensin II
ANTadenine-nucleotide translocase
Apaf-1apoptosis activation factor-1
ARDSacute respiratory distress syndrome
AREantioxidant response element
ASCapoptosis-associated speck-like protein
BH4tetrahydrobiopterin
CAMscell adhesion molecules
CCcoiled-coil
CD99L2CD99 antigen like 2
CLcardiolipin
CTDC-terminal domain
Cyt-cCytochrome-c
DAGdiacylglycerol
DAMPdanger-associated molecular pattern
DCsdendritic cells
DISCdeath-inducing signaling complex
eNOSendothelial NOS
ESAMendothelial cell-selective adhesion molecule
ESL-1E-selectin ligand-1
ETCelectron transport chain
F-actinfilamentous actin
FADflavin-adenine dinucleotide
FADDFas-associated death domain
GEFguanine nucleotide exchange factor
GMP-140granule membrane protein-140
GPxglutathione peroxidase
GSHglutathione
GUKguanylate kinase
H2O2hydrogen peroxide
HEVshigh endothelial venules
HOClhypochlorous acid
ICAM-1intercellular adhesion molecule-1
IEJsinter-endothelial junctions
IL-1interleukin-1
iNOSinducible NOS
JAMsjunctional adhesion molecules
JMDjuxtamembrane domain
Keap1Kelch-like ECH-associated protein 1
LFA-1leukocyte function–associated antigen 1
LPSlipopolysaccharide
MDCKMadin Darby Canine Kidney
MLCKmyosin light chain kinase
MnSODmanganese SOD
MOMPmitochondrial outer membrane permeability
MPTmitochondrial permeability transition
mPTPmitochondrial permeability transition pore
MtROSmitochondrial derived ROS
NACN-acetyl cysteine
NLRnod like receptors
nNOSneuronal NOS
NOnitric oxide
NOSnitric oxide synthase
Nrf2NF-E2-related factor 2
OHhydroxyl radical
PAFplatelet activating factor
PAMPpathogen-associated molecular pattern
PMNspolymorphonuclear neutrophils
PRRspattern-recognition receptors
PSphosphatidylserine
PSGL-1P-selectin glycoprotein ligand-1
RIP1receptor-interacting kinase 1
RNSreactive nitrogen species
ROSreactive oxygen species
SODsuperoxide dismutase
TBP-2thioredoxin-binding protein-2
TEMstetraspanin-enriched microdomains
TIRToll/IL-1R
TJstight junctions
TLRsToll-like receptors
TNFR1TNF-α receptor–1
TRAF2TNFα-receptor-associated factor 2
TRAIL-R1TNF-related apoptosis-inducing ligand receptor 1
TRAPStumor necrosis factor receptor-associated periodic syndrome
Trxthioredoxin
VCAM-1vascular cell adhesion molecule-1
VDACvoltage-dependent anion channels
VDUP1vitamin D3 up-regulated protein 1
VLA4very late antigen 4
XDHxanthine dehydrogenase
XOxanthine oxidase
Abbreviations Used

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