Toll-like receptors in ischemia-reperfusion injury

Thiruma V. Arumugam, Eitan Okun, Sung Chun Tang, John Thundyil, Stephen M. Taylor, Trent M. Woodruff

Research output: Contribution to journalReview articlepeer-review

271 Scopus citations

Abstract

Ischemia-reperfusion (I/R) injuries are implicated in a large array of pathological conditions such as myocardial infarction, cerebral stroke, and hepatic, renal, and intestinal ischemia, as well as following cardiovascular and transplant surgeries. The hallmark of these pathologies is excessive inflammation. Toll-like receptors (TLRs) are recognized as one of the main contributors to pathogen-induced inflammation and, more recently, injury-induced inflammation. Endogenous ligands such as low-molecular hyaluronic acid, fibronectin, heat shock protein 70, and heparin sulfate were all found to be cleaved in the inflamed tissue and to activate TLR2 and TLR4, initiating an inflammatory response even in the absence of pathogens and infiltrating immune cells. In this review, we discuss the contribution of TLR activation in hepatic, renal, cerebral, intestinal, and myocardial I/R injuries. A greater understanding of the role of TLRs in I/R injuries may aid in the development of specific TLR-targeted therapeutics to treat these conditions.

Original languageEnglish
Pages (from-to)4-16
Number of pages13
JournalShock
Volume32
Issue number1
DOIs
StatePublished - Jul 2009
Externally publishedYes

Keywords

  • Apoptosis
  • Ischemia-reperfusion injury
  • Myocardial infarction
  • Neuron
  • Stroke
  • Toll-like receptors

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