Endothelial Cell Perturbation and Low‐Density Lipoprotein

Abstract

The focal entry and accumulation of LDL within the arterial wall of the normal animal may represent an early stage in the development of the atherosclerotic plaque. Concentrations of LDL 10 to 100 times normal medial concentrations might be difficult to clear from the arterial wall, permitting accumulation of lipid. Elevated LDL concentrations, in proximity to smooth muscle cells, appear to stimulate SMC proliferation. High LDL concentrations might also enhance mononuclear cell adhesion to endothelium. Since LDL has a high affinity for heparin and heparin for growth factors, LDL accumulation may be a mechanism for the concentration of such materials in the intima. The observation of markedly enhanced macromolecular permeability foci could be related to several potential mechanisms of initiation of atherosclerosis. This observation is of particular note when the focal occurrence of atherosclerosis is considered. Although atherosclerosis is seen as a generalized thickening of the intima, it is the focal narrowing of the lumen that is often responsible for the stenosis which produces symptoms such as angina or myocardial infarction.