Chappey O, Dosquet C, Wautier M P, Wautier J L
Biologie Vasculaire et Cellulaire, Immunohematologie, Hôpital Lariboisiere, Paris VII, France.
Eur J Clin Invest. 1997 Feb;27(2):97-108. 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.
在糖尿病和衰老等与血管疾病相关的病症中可观察到晚期糖基化终产物（AGEs）的形成。AGEs通过醛糖与蛋白质的NH2相互作用形成，随后的阿马多里重排导致形成复杂分子。AGE分子的异质类存在于血浆、细胞和组织中，并在血管壁和肾脏中积累。AGE反应可产生活性氧中间体（ROIs），其可作为信号介质，并且对分子或细胞可能是有害的。AGEs和ROI诱导的细胞功能障碍可干扰调节细胞增殖和血管功能的肽和细胞因子的基因表达。AGEs与AGE受体（RAGE）相互作用后会发生一系列细胞内修饰，这可能与动脉粥样硬化的发展有关。通过适当治疗尽量减少AGE形成并限制ROI产生的尝试可能会导致糖尿病患者血管疾病的减轻或进展减缓。
