Weinbaum S, Chien S
Department of Mechanical Engineering, City College of the City University of New York, NY 10031.
J Biomech Eng. 1993 Nov;115(4B):602-10. doi: 10.1115/1.2895547.
In this review we shall examine the current understanding of events that lead to the incipient formation of the early foam cell lesion in atherogenesis and its localization. Particular emphasis will be placed on the intimal transport mechanisms that lead to the growth of extracellular lipid liposomes in the intima, since there is now substantial evidence that this growth is the triggering event in the complex sequence of processes that leads to the recruitment of blood borne monocytes into the subendothelial intima and their subsequent conversion to macrophages. The role of the endothelium, intimal proteoglycans and internal elastic lamina (IEL) in modulating the transport of low density lipoproteins (LDL) in the subendothelial space will be analyzed and a new hypothesis for the co-localization of liposome formation, cellular level endothelial leakage and monocyte entry described. The possible modifications of LDL in the liposomes that facilitate the conversion of monocytes into foam cells is summarized. We also discuss the fluid dynamic aspects of intimal transport and the relationship of fluid shear stress to the localization of cellular level endothelial leakage of LDL. The effect of fluid shear on other endothelial cell functions has been recently reviewed in [1].
在本综述中，我们将探讨目前对动脉粥样硬化早期泡沫细胞病变起始形成及其定位相关事件的理解。将特别强调导致内膜中细胞外脂质脂质体生长的内膜转运机制，因为现在有大量证据表明，这种生长是导致血源性单核细胞募集到内皮下内膜并随后转化为巨噬细胞的复杂过程序列中的触发事件。将分析内皮、内膜蛋白聚糖和内弹性膜（IEL）在调节内皮下空间中低密度脂蛋白（LDL）转运方面的作用，并描述脂质体形成、细胞水平内皮渗漏和单核细胞进入共定位的新假说。总结了脂质体中LDL可能的修饰，这些修饰促进单核细胞转化为泡沫细胞。我们还讨论了内膜转运的流体动力学方面以及流体剪切应力与LDL细胞水平内皮渗漏定位的关系。流体剪切对其他内皮细胞功能的影响最近已在[1]中进行了综述。
