Advanced glycation end products, oxidant stress and vascular lesions

• Published in: European journal of clinical investigation Vol. 27; no. 2; pp. 97 - 108
• Main Authors: CHAPPEY, O., DOSQUET, C., WAUTIER, M-P., WAUTIER, J-L.
• Format: Journal Article
• Language: English
• Published: Oxford BSL Blackwell Science Ltd 01.02.1997; Blackwell
• Subjects: Animals; Associated diseases and complications; Atherosclerosis; Biological and medical sciences; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Diabetic Angiopathies - physiopathology; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; endothelial cells; glycation; Glycation End Products, Advanced - adverse effects; Glycation End Products, Advanced - biosynthesis; Glycation End Products, Advanced - metabolism; Glycosylation; Humans; Medical sciences; monocytes; oxidant stress; Oxidants - adverse effects; Oxidants - metabolism; Reactive Oxygen Species - metabolism; Reactive Oxygen Species - physiology; Vascular Diseases - etiology; Vascular Diseases - physiopathology; Endocrinopathy; Vascular disease; Human; Oxidative stress; Pathogenesis; Diabetes mellitus; Atherosclerosis; Cardiovascular disease; Complication; Glycation
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1046/j.1365-2362.1997.710624.x

The formation of advanced glycation end products (AGEs) is observed in conditions such as diabetes mellitus and ageing, both associated with vascular disorders. AGEs form by the interaction of an aldose with NH2 of proteins, and the subsequent Amadori rearrangement leads to complex molecules. The heterogeneous class of AGE molecules is found in plasma, cells and tissues and accumulates in the vessel wall and the kidney. AGE reactions can generate reactive oxygen intermediates (ROIs), which can act as signal mediators and can be deleterious for molecules or cells. The AGEs and ROI‐induced cellular dysfunctions can interfere with the gene expression of peptides and cytokines regulating cell proliferation and vascular functions. The interaction of AGEs with the AGE receptor (RAGE) is followed by a series of intracellular modifications that may be involved in the development of atherosclerosis. An attempt to minimize AGE formation and to limit ROI production by an appropriate therapy may result in the reduction or slowing of vascular disease in patients with diabetes mellitus.