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Mediators of Inflammation
Volume 2010, Article ID 704202, 8 pages
Review Article

TLR2 and TLR4 in Ischemia Reperfusion Injury

1Laboratory of Experimental Cardiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
2Opsona Therapeutics Ltd., Institute of Molecular Medicine, Trinity Centre for Health Sciences, St. James' Hospital, Dublin 8, Ireland

Received 22 March 2010; Accepted 7 April 2010

Academic Editor: Philipp M. Lepper

Copyright © 2010 F. Arslan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Ischemia reperfusion (I/R) injury refers to the tissue damage which occurs when blood supply returns to tissue after a period of ischemia and is associated with trauma, stroke, myocardial infarction, and solid organ transplantation. Although the cause of this injury is multifactorial, increasing experimental evidence suggests an important role for the innate immune system in initiating the inflammatory cascade leading to detrimental/deleterious changes. The Toll-like Receptors (TLRs) play a central role in innate immunity recognising both pathogen- and damage-associated molecular patterns and have been implicated in a range of inflammatory and autoimmune diseases. In this paper, we summarise the current state of knowledge linking TLR2 and TLR4 to I/R injury, including recent studies which demonstrate that therapeutic inhibition of TLR2 has beneficial effects on I/R injury in a murine model of myocardial infarction.