Bourajjaj M, Stehouwer C D A, van Hinsbergh V W M, Schalkwijk C G
Department of Clinical Chemistry, Institute for Cardiovascular Research, VU University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.
Biochem Soc Trans. 2003 Dec;31(Pt 6):1400-2. doi: 10.1042/bst0311400.
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.
人们提出了各种理论来解释高血糖诱导的糖尿病血管并发症的发病机制,包括晚期糖基化终产物(AGEs)对血管组织的有害影响。糖酵解的副产物之一、反应性很强的二羰基化合物甲基乙二醛(MGO)生成增加,且由MGO衍生的AGEs似乎与糖尿病血管并发症的发生有关。尽管MGO及其加合物在血管并发症发生过程中的确切作用尚不清楚,但MGO-精氨酸加合物水解咪唑啉酮介导的血管细胞受体激活以及MGO对蛋白质的细胞内修饰似乎都与之有关。本综述的目的是评估MGO在多大程度上与糖尿病血管并发症相关。