Curtiss Linda K, Tobias Peter S
Department of Immunology and Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
J Lipid Res. 2009 Apr;50 Suppl(Suppl):S340-5. doi: 10.1194/jlr.R800056-JLR200. Epub 2008 Nov 1.
Atherosclerosis is inflammation of the vessel wall of the arterial tree. This inflammation arises at specific areas that experience disturbed blood flow such as bifurcations and the lesser curvature of the aortic arch. Although all endothelial cells are exposed to comparable levels of circulating plasma cholesterol, only endothelial cells overlaying lesions display an inflamed phenotype. This occurs even in the absence of any additional exacerbating disease factors because blood flow controls the expression of Toll-like receptors (TLR), which are initiators of cellular activation and inflammation. TLR2- and 4-expression exert an overall proatherogenic effect in hyperlipidemic mice. TLR activation of the endothelium promotes lipid accumulation and leukocyte accumulation within lesions.
动脉粥样硬化是动脉血管壁的炎症。这种炎症出现在血流紊乱的特定区域,如分叉处和主动脉弓的小弯处。尽管所有内皮细胞都暴露于循环血浆胆固醇的相当水平,但只有覆盖病变的内皮细胞表现出炎症表型。即使在没有任何其他加重疾病因素的情况下也会发生这种情况,因为血流控制着Toll样受体(TLR)的表达,而TLR是细胞活化和炎症的启动因子。TLR2和4的表达在高脂血症小鼠中具有总体促动脉粥样硬化作用。内皮细胞的TLR激活促进病变内脂质和白细胞的积聚。