Mechanisms of cholesterol accumulation in the arterial wall.
The rate of cholesterol accumulation is a function of three separate processes: the transfer of lipid or lipoprotein from blood plasma to the artery, the binding and sequestering of lipids in the arterial wall and the solubilization and removal of lipid from the artery. These processes have been studied with lipids or lipoproteins labeled with radioisotopes by autoradiographic and quantitative chemical procedures. More recently immunochemical procedures have been applied to this problem. Studies have been performed with intact animals, isolated organs and cell cultures. In addition, homogenates have been used successfully to study intraarterial transformations of lipids, (for example, cholesterol esterification). Although epidemiologic and clinical studies, as well as animal experiments, have provided evidence that the concentration of plasma low or very low density lipoproteins parallels the rate of atherogenesis, the nature of the causal chain linking plasma lipoproteins to atherosclerosis is as yet unclear. A possible link between plasma lipoproteins, arterial liproprotein lipase and atherogenesis has been postulated.
D000818:Animals; D001158:Arteries / Q000378:metabolism*; D001161:Arteriosclerosis / Q000201:enzymology / Q000209:etiology / Q000378:metabolism*; D002250:Carbon Radioisotopes; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D002914:Chylomicrons / Q000378:metabolism; D004952:Esters; D005227:Fatty Acids / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D006867:Hydrolases / Q000378:metabolism; D008074:Lipoproteins / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D012107:Research Design; D014316:Tritium
D002250:Carbon Radioisotopes; D002914:Chylomicrons; D004952:Esters; D005227:Fatty Acids; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D014316:Tritium; D002784:Cholesterol; D006867:Hydrolases