Lipoproteins, platelets, and prostaglandins in atherosclerosis
| Autor: | Peter T. Kuo |
|---|---|
| Rok vydání: | 1981 |
| Předmět: |
Blood Platelets
medicine.medical_specialty Arteriosclerosis Population Coronary Disease Familial hypercholesterolemia Coronary artery disease chemistry.chemical_compound Internal medicine medicine Humans Platelet activation education education.field_of_study Cholesterol business.industry Cell Membrane medicine.disease Lipoproteins LDL Endocrinology chemistry Low-density lipoprotein LDL receptor Prostaglandins lipids (amino acids peptides and proteins) Lipoproteins HDL Cardiology and Cardiovascular Medicine business Lipoprotein |
| Zdroj: | American Heart Journal. 102:949-953 |
| ISSN: | 0002-8703 |
| DOI: | 10.1016/0002-8703(81)90056-9 |
| Popis: | It is generally believed that atherosclerosis is a disease of multiple interacting causative factors and its prevention or control requires intervention in several parameters. Discussion presented in this communication is focused on the aspect of interaction between lipid-lipoprotein metabolism, platelet activation, prostaglandin (PG)-metabolite production and their association with atherosclerosis. Hypercholesterolemia (LDL elevation) in atherosclerosis. Experimental, epidemiologic, and clinical studies have identified hypercholesterolemia, or low density lipoprotein (LDL) elevation, as a major risk factor of coronary artery disease (CAD),l-” although a cause-effect relationship cannot be established. Through general population surveys, it appears that an increase of the major cholesterol transporting lipoprotein, LDL, is positively correlated with atherogenesis2 By genetic analysis, type II hyperlipoproteinemia, or familial hypercholesterolemia (FH), has been clearly defined and shown to carry a greatly increased risk of premature and accelerated CAD.“-” Goldstein and BrownlO have employed cellular biology technology to elucidate the LDL-cell interaction in these highly atherosclerotic prone FH patients. The cells from FH patients are found to lack or be deficient in the high-affinity LDL receptors. This cellular deficit is mainly responsible for LDL elevation and its associated hypercholesterolemia. Several mechanisms may be invoked to relate high and low density plasma lipoprotein species with different aspects of atherosclerosis. Some of the more persuasive ones are presented herein. Antiatherogenic HDL effects. Since the peripheral tissue cells are incapable of degrading cholesterol, to |
| Databáze: | OpenAIRE |
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