TLR2 and TLR4 in Ischemia Reperfusion Injury

Joint Authors

Parker, Andrew E.
Arslan, Fatih
Keogh, B.
McGuirk, P.

Source

Mediators of Inflammation

Issue

Vol. 2010, Issue 2010 (31 Dec. 2010), pp.1-8, 8 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2010-06-09

Country of Publication

Egypt

No. of Pages

8

Main Subjects

Diseases

Abstract EN

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.

American Psychological Association (APA)

Arslan, Fatih& Keogh, B.& McGuirk, P.& Parker, Andrew E.. 2010. TLR2 and TLR4 in Ischemia Reperfusion Injury. Mediators of Inflammation،Vol. 2010, no. 2010, pp.1-8.
https://search.emarefa.net/detail/BIM-491903

Modern Language Association (MLA)

Arslan, Fatih…[et al.]. TLR2 and TLR4 in Ischemia Reperfusion Injury. Mediators of Inflammation No. 2010 (2010), pp.1-8.
https://search.emarefa.net/detail/BIM-491903

American Medical Association (AMA)

Arslan, Fatih& Keogh, B.& McGuirk, P.& Parker, Andrew E.. TLR2 and TLR4 in Ischemia Reperfusion Injury. Mediators of Inflammation. 2010. Vol. 2010, no. 2010, pp.1-8.
https://search.emarefa.net/detail/BIM-491903

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-491903