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      Linking oxidative stress to inflammation: Toll-like receptors

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      Free Radical Biology and Medicine

      Elsevier BV

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          Abstract

          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) 2009 Elsevier Inc. All rights reserved.

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          Author and article information

          Journal
          Free Radical Biology and Medicine
          Free Radical Biology and Medicine
          Elsevier BV
          08915849
          May 01 2010
          May 01 2010
          : 48
          : 9
          : 1121-1132
          10.1016/j.freeradbiomed.2010.01.006
          3423196
          20083193
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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