Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 48, Issue 9, Pages 1121-1132Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2010.01.006
Keywords
Toll-like receptor; Redox stress; DAMPs; HMGB1; Ischemia/reperfusion; Hemorrhagic shock; NADPH oxidase; Free radicals
Funding
- NIGMS NIH HHS [R01 GM050441, R01 GM050441-09] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM050441] Funding Source: NIH RePORTER
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Injury caused by oxidative stress occurs in many clinical scenarios involving ischemia and reperfusion such as organ transplantation, hemorrhagic shock (HS), myocardial infarction, and cerebral vascular accidents. Activation of the immune system as a result of disturbances-in the redox state of cells seems to contribute to tissue and organ damage in these conditions. The link between oxidative stress and inflammatory pathways is poorly understood. Recently, Toll-like receptors (TLRs) have been shown to mediate the inflammatory response seen in experimental ischemia and reperfusion (I/R). The TLR family of receptors involved in alerting the innate immune system of danger seems to be activated by damage-associated molecular pattern molecules (DAMPS) that are released during conditions of oxidative stress. In this review, we examine the role of TLRs in various experimental models of oxidative stress such as HS and I/R. We also report on potential DAMPs that may interact with TLRs in mediating injury. Finally, potential mechanisms by which reactive oxygen species from NADPH oxidase can signal the commencement of inflammatory pathways through TLRs are explored. (C) 2010 Elsevier Inc. All rights reserved.
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