Department of Cardiovascular Sciences, Leicester University, Glenfield General Hospital, Leicester, UK.
J Innate Immun. 2009;1(4):340-9. doi: 10.1159/000191413. Epub 2009 Jan 8.
Atherosclerosis is a chronic inflammatory disease of the arteries that is characterised by the activation of endothelial cells, the recruitment of monocytes into the vessel wall and the differentiation of recruited macrophages into cholesterol-laden foam cells. Recent evidence from a variety of experimental approaches has indicated that Toll-like receptors (TLRs), which serve to initiate inflammatory signalling in response to the detection of molecules associated with microbial infection or tissue damage, play key roles in the development of atherosclerosis. This review summarises the recent evidence implicating TLR-dependent signalling in the activation of vascular cells during atherogenesis, and the mechanisms by which TLR-signalling may promote the dysregulation of macrophage cholesterol metabolism that is a prerequisite for the formation of foam cells and lesion progressionin vivo. Particular attention is paid to the recent studies aimed at identifying potential ligands of the TLRs that may be relevant to atherogenesis, and the diverse mechanisms by which vascular tissues may become exposed to ligands of the TLRs.
动脉粥样硬化是一种动脉的慢性炎症性疾病,其特征在于内皮细胞的激活、单核细胞募集到血管壁以及募集的巨噬细胞分化为富含胆固醇的泡沫细胞。最近,各种实验方法的证据表明,Toll 样受体 (TLR) 在检测与微生物感染或组织损伤相关的分子时,可启动炎症信号转导,在动脉粥样硬化的发生发展中发挥关键作用。这篇综述总结了最近的证据,表明 TLR 依赖性信号转导在动脉粥样形成过程中血管细胞的激活,以及 TLR 信号转导如何促进巨噬细胞胆固醇代谢的失调,这是泡沫细胞形成和体内病变进展的前提。特别关注的是最近旨在确定可能与动脉粥样硬化相关的 TLR 潜在配体的研究,以及血管组织可能接触 TLR 配体的多种机制。