Lipid markers for atherosclerosis.
Atherogenesis results from the simultaneous occurrence of 2 important processes: platelet-endothelial interaction, with its consequences mediated by the platelet-derived growth factor, and lipid accumulation. Lipid accumulation results from the balance or imbalance of cellular uptake of lipoproteins versus the removal of cholesterol esters. Uptake results from activity of the low-density lipoprotein (LDL) receptor of smooth muscle cells and fibroblasts, modified LDL receptor and remnant receptors of macrophages. Cholesterol-ester removal is regulated by apolipoprotein A-l. Low levels of apolipoprotein A-l are found in most patients with clinically significant coronary artery disease, suggesting that defects in cellular cholesterol ester removal may play an important role in atherogenesis.
Kottke
B A
BA
D016632:Apolipoprotein A-I; D001054:Apolipoproteins A / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism; D001665:Binding Sites; D002784:Cholesterol / Q000378:metabolism; D004727:Endothelium / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000378:metabolism; D008264:Macrophages / Q000502:physiology; D011973:Receptors, LDL / Q000032:analysis
D016632:Apolipoprotein A-I; D001054:Apolipoproteins A; D008074:Lipoproteins; D011973:Receptors, LDL; C036053:VLDL receptor; D002784:Cholesterol