Development of atherosclerotic plaques.
Atherosclerosis is a multifactorial disease. A unified model for the lesion development reveals many connections between the response-to-injury hypothesis and the lipid hypothesis. Various cellular uptake mechanisms for native and modified lipoproteins are discussed with respect to foam cell formation and lesion development. The role of arterial smooth muscle cells in atherogenesis is emphasized. Preliminary results of biochemical analyses from the coronary arteries of accidentally died Finnish children and adults reveal that the accumulation of plasma-derived cholesteryl esters in young children began early in childhood, long before the vessels became macroscopically affected and changes in arterial glycosaminoglycans correlated significantly with the accumulation of cholesteryl esters.
D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division; D002788:Cholesterol Esters / Q000032:analysis; D003238:Connective Tissue / Q000378:metabolism; D003331:Coronary Vessels / Q000032:analysis; D004848:Epithelium / Q000502:physiology; D005487:Foam Cells / Q000378:metabolism; D006025:Glycosaminoglycans / Q000032:analysis; D006801:Humans; D050356:Lipid Metabolism; D008077:Lipoproteins, LDL / Q000097:blood; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011817:Rabbits
D002788:Cholesterol Esters; D006025:Glycosaminoglycans; D008077:Lipoproteins, LDL