[Lipids and blood vessels].
The key lesion in atherosclerosis is termed atheroma. It consists of intracellular and extracellular cholesterol esters. Because atheromas are located subendothelially, an interrelation with blood cholesterol has long been suspected. In the blood, cholesterol is wrapped in lipoproteins, with the largest amount being found in low-density lipoproteins (LDL), whereas a smaller amount is found in high-density lipoproteins (HDL). LDL (and their cholesterol) are removed from the plasma by receptor-mediated uptake. Impaired LDL-receptor interaction results in accumulation of LDL in plasma. LDL now penetrate the endothelial layer and become deposited in the arterial intima. This process initiates atheroma formation. Excess tissue cholesterol (e.g. in the arterial intima) is returned to the liver by HDL. The HDL2 subfraction is particularly effective in this reverse cholesterol transport. Patients with coronary atherosclerosis either have a defect in reverse cholesterol transport (i.e. low HDL2 levels) or an excess in cholesterol load (i.e. high LDL). The ratio between LDL and HDL2 cholesterol determines the risk for atherosclerotic disease. Triglycerides lower HDL2 levels and thereby exert indirect atherogenicity.
Drexel
H
H
Departement für Innere Medizin, Universitätsspital Zürich.
Amann
F W
FW
D001161:Arteriosclerosis / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D011973:Receptors, LDL / Q000378:metabolism
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008074:Lipoproteins; D011973:Receptors, LDL
Lipide und Blutgefässe.