Laboratory of Experimental Cardiology, University Medical Center Utrecht, Heidelberglaan 100, Utrecht, The Netherlands.
Mediators Inflamm. 2010;2010:704202. doi: 10.1155/2010/704202. Epub 2010 Jun 9.
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.
缺血再灌注(I/R)损伤是指组织在缺血一段时间后恢复血液供应时发生的组织损伤,与创伤、中风、心肌梗死和实体器官移植有关。尽管这种损伤的原因是多因素的,但越来越多的实验证据表明,先天免疫系统在启动导致有害/有害变化的炎症级联反应中起着重要作用。Toll 样受体(TLRs)在先天免疫中起着核心作用,既能识别病原体相关分子模式,又能识别损伤相关分子模式,并与一系列炎症和自身免疫性疾病有关。在本文中,我们总结了将 TLR2 和 TLR4 与 I/R 损伤联系起来的现有知识,包括最近的研究表明,在心肌梗死的小鼠模型中,TLR2 的治疗性抑制对 I/R 损伤有有益的影响。