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TLR2 and TLR4 in Ischemia Reperfusion Injury

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 exp...

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Detalles Bibliográficos
Autores principales: Arslan, F., Keogh, B., McGuirk, P., Parker, A. E.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902053/
https://www.ncbi.nlm.nih.gov/pubmed/20628516
http://dx.doi.org/10.1155/2010/704202
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author Arslan, F.
Keogh, B.
McGuirk, P.
Parker, A. E.
author_facet Arslan, F.
Keogh, B.
McGuirk, P.
Parker, A. E.
author_sort Arslan, F.
collection PubMed
description 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.
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spelling pubmed-29020532010-07-13 TLR2 and TLR4 in Ischemia Reperfusion Injury Arslan, F. Keogh, B. McGuirk, P. Parker, A. E. Mediators Inflamm Review Article 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. Hindawi Publishing Corporation 2010 2010-06-09 /pmc/articles/PMC2902053/ /pubmed/20628516 http://dx.doi.org/10.1155/2010/704202 Text en Copyright © 2010 F. Arslan et al. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Review Article
Arslan, F.
Keogh, B.
McGuirk, P.
Parker, A. E.
TLR2 and TLR4 in Ischemia Reperfusion Injury
title TLR2 and TLR4 in Ischemia Reperfusion Injury
title_full TLR2 and TLR4 in Ischemia Reperfusion Injury
title_fullStr TLR2 and TLR4 in Ischemia Reperfusion Injury
title_full_unstemmed TLR2 and TLR4 in Ischemia Reperfusion Injury
title_short TLR2 and TLR4 in Ischemia Reperfusion Injury
title_sort tlr2 and tlr4 in ischemia reperfusion injury
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902053/
https://www.ncbi.nlm.nih.gov/pubmed/20628516
http://dx.doi.org/10.1155/2010/704202
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