Glycation and Oxidation of Proteins: A Role in the Pathogenesis of Atherosclerosis?

摘要: Glycation affects any protein exposed to glucose. In long-lived proteins, further reactions lead unreactive advanced glycation end-products (AGE). Although numerous, the structures of only two AGE products, carboxymethyllysine (CML) and pentosidine, are known. formation involves sequential free radical oxidation reactions: thus these products may be termed “glycoxidation products”. Both glycoxidation important in development atherosclerosis, an increase either glycative or oxidative stress promote this disease. LDL impairs its recognition by receptor, stimulates cholesteryl ester (CE) synthesis macrophages (promoting hyperlipidemia foam cell formation), enhances platelet aggregation. covalent binding lipoproteins vascular wall promoting sequestration. cause release, hence damage lipids, apolipoproteins, nearby macromolecules. Patients with significant whether diabetic not, tend have increased peroxidation plasma lipids. Even if a result, not cause, initial injury, lipid peroxides vessel walls through cytotoxicity endothelial smooth muscle cells.