Implications of the monoclonal character of human atherosclerotic plaques.
Evidence for the monoclonal nature of human atherosclerotic plaques is reviewed. Eighty percent of discrete raised atherosclerotic plaques are of single phenotype. Interpretations alternative to single-cell orgin, based on patch size, selection due to linked genes, or repetitive sampling do not seem to explain the apparent monoclonality. Search for carriers in serum of mutagens, such as may be present in cigarette smoke, show them to be the lipoproteins, and the presence and possible role of intrinsic mutagens, e.g., cholesterol-alpha-oxide, are presented. The possible role for other factors implied by the monoclonal hypothesis, e.g., the mechanism by which estrogen therapy may increase coronary attacks, is discussed.
D000273:Adipose Tissue / Q000166:cytology; D000293:Adolescent; D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000201:enzymology / Q000209:etiology* / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D002999:Clone Cells; D004967:Estrogens / Q000009:adverse effects; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007527:Isoenzymes; D008074:Lipoproteins / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009130:Muscle, Smooth / Q000166:cytology; D009153:Mutagens; D010641:Phenotype
D004967:Estrogens; D007527:Isoenzymes; D008074:Lipoproteins; D009153:Mutagens; D005954:Glucosephosphate Dehydrogenase