Various theories have been proposed to explain the hyperglycaemia-induced pathogenesis of vascular complications of diabetes, including detrimental effects of AGEs (advanced glycation end products) on vascular tissues. Increased formation of the very reactive dicarbonyl compound MGO (methylglyoxal), one of the side-products of glycolysis, and MGO-derived AGEs seem to be implicated in the development of diabetic vascular complications. Although the exact role of MGO and MGO adducts in the development of vascular complications is unknown, receptor-mediated activation of vascular cells by the MGO–arginine adduct hydroimidazolone, as well as intracellular modifications of protein by MGO, seem to be involved. The aim of this mini-review is to assess to what extent MGO is related to vascular complications in diabetes.

Abbreviations used: AGE, advanced glycation end product; CEL, N-(1-carboxyethyl)lysine; CML, N-(carboxymethyl)lysine; ERK, extracellular-signal-regulated kinase; Hsp, heat-shock protein; MAPK, mitogen-activated protein kinase; MGO, methylglyoxal; MOLD, methylglyoxal–lysine dimer; NF-κB, nuclear factor-κB; RAGE, receptor for AGEs.

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Author notes

679th Meeting of the Biochemical Society held at the University of Essex, Colchester, 2–4 July 2003