New morphological and biochemical aspects of atherosclerosis.
According to morphological and biochemical findings, disturbances of metabolism (turnover) and function of smooth muscle cells and proteoglycans/GAG are decisive for the development of early and progressive atherosclerotic changes. The feedback dependencies between the smooth muscle cells and the components of the extracellular substance demonstrated, permit to call primary target points of atherogenic injuries of al constituents of this regulating circle system. If the increased turnovers of the arterial components do not return to a normal equilibrium, the result is hyperplasia of the cellular and intercellular constituents. The early atherosclerotic lesions can progress or relapse. In late and regressive lesions, the cell content as well as the anabolic and esp. the catabolic processes decrease. There result scars rich in collagen fibres and poorer in cells, ground substance, and elastin. The healing of atherosclerotic lesions can take place in any stage, the later the more difficult and insufficient. Disturbances of the fat metabolism, the own synthesis, and the intake of substances by smooth muscle and hematogenic cells are secondary sequels of the primary early atherosclerotic alterations and might be regarded as metabolic lesion of the smooth muscle cells. Other secondary and tertiary processes (calcification, fibrous degeneration, esp. of elastin) support the hypothesis that the early atherosclerotic lesions and their progress may finally start and perpetuate a metabolic insufficiency of the arterial wall.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D001158:Arteries / Q000378:metabolism / Q000473:pathology; D001161:Arteriosclerosis / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division; D004247:DNA / Q000032:analysis; D004261:DNA Replication; D006801:Humans; D006965:Hyperplasia; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D051381:Rats; D013045:Species Specificity
D004247:DNA