Implications of the monoclonal character of human atherosclerotic plaques.
The evidence for the monoclonal nature of human atherosclerotic plaques is briefly reviewed. The interpretation of the cellular monotypy found in a large percentage (75 to 80%) of discrete raised atherosclerotic plaques as being monoclonal in origin appear firm since the size of patches of cells of the same type appears to be very small (ca. 10(-4) cu mm and 10 +/- cells). Evidence for explanations other than single cell origins of each plaque do not appear, at the moment, to be compelling. If we assume then that there is reason to accept the monoclonal character of atherosclerotic plaques in human beings then we are led to a search for the presence of factors that could "initiate" the monoclonal proliferation as well as factors that may promote the growth of the plaques. Evidence is presented that increased risk of atherosclerosis found with cigarette smoking is due to absorption from the lung and circulation in the blood of aryl hydrocarbons. Experiments show that these are preferentially carried in the same parts of the serum that transport cholesterol. The possibility of intrinsic initiators derived from cholesterol is discussed. A possible mechanism for the role of hypertension in promoting atherosclerosis is considered. Finally the evidence for a possible role of viruses in the pathogenesis of atherosclerosis is discussed.
D001161:Arteriosclerosis / Q000209:etiology* / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D002999:Clone Cells / Q000201:enzymology; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000032:analysis; D006801:Humans; D009153:Mutagens; D010641:Phenotype; D011083:Polycyclic Compounds / Q000097:blood; D012907:Smoking / Q000150:complications
D009153:Mutagens; D011083:Polycyclic Compounds; D002784:Cholesterol; D005954:Glucosephosphate Dehydrogenase