[Studies on the pathogenesis of atherosclerosis].
Studies on the pathogenesis of atherosclerosis (As) were reviewed in our institute. Clinico-pathological study showed that coronary As lesions appeared early and took a long-time to seriously stenosis the arterial lumen, resulting in coronary heart disease. Studies on human As lesions by light and electron microscopy suggested that injury to and increased permeability of endothelial cells (EC) and proliferation of smooth muscle cells (SMC), together with an increase of proteoglycans(PG) were important in atherogenesis. Morphologic responses of the aortic wall of normally fed rats to intimal injury by an indwelling catheter (in place for 3 weeks) were studied at the time of removal of the catheter and 4, 8, and 26 weeks later. Neointimal thickening with SMC proliferation and a significant increase in chondroitin sulfate (CS)-PG granule concentrations were found. A study on cultured human EC showed that after EC reached confluence, secretion of heparin sulfate (HS)-PG increased and inhibited the proliferation of SMC. The proliferative ability of cultured human SMC was found to decrease after 8 passages. More lipid accumulation was found in SMC's of the 10th passage (T10) than in those of the 4th passage (T4). T10 SMC showed a higher 35S incorporation into dermatan sulfate (DS) CS-PG than did T4 SMC in both the medium and cell layer. The results suggest that SMC senescence may play an important role in the pathogenesis of As.
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D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000209:etiology* / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats
D011509:Proteoglycans