TLR2 and TLR4 in ischemia reperfusion injury.

TLR2 and TLR4 in ischemia reperfusion injury.
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DOI:
10.1155/2010/704202
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发表时间:
2010
影响因子:
4.6
通讯作者:
Parker AE
Parker AE
中科院分区:
医学3区
文献类型:
--
作者:
Arslan F;Keogh B;McGuirk P;Parker AE

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缺血再灌注(I/R)损伤是指在缺血一段时间后当血液供应返回组织时发生的组织损伤,并且与创伤、中风、心肌梗死和实体器官移植相关。虽然这种损伤的原因是多因素的,但越来越多的实验证据表明先天免疫系统在引发导致有害/有害变化的炎症级联反应中起重要作用。Toll样受体(TLR)在先天免疫中起着核心作用,识别病原体和损伤相关的分子模式,并与一系列炎症和自身免疫性疾病有关。在本文中,我们总结了目前的知识状态TLR 2和TLR 4连接到I/R损伤,包括最近的研究表明,治疗性抑制TLR 2对I/R损伤的小鼠模型心肌梗死的有益影响。
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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