Stirban Alin, Gawlowski Thomas, Roden Michael
Profil Institut für Stoffwechselforschung GmbH, Hellersbergstrasse 9, 41460 Neuss, Germany.
University of Paderborn, Warburger Str. 100, 33098 Paderborn, Germany.
Mol Metab. 2013 Dec 7;3(2):94-108. doi: 10.1016/j.molmet.2013.11.006. eCollection 2014 Apr.
The enhanced generation and accumulation of advanced glycation endproducts (AGEs) have been linked to increased risk for macrovascular and microvascular complications associated with diabetes mellitus. AGEs result from the nonenzymatic reaction of reducing sugars with proteins, lipids, and nucleic acids, potentially altering their function by disrupting molecular conformation, promoting cross-linking, altering enzyme activity, reducing their clearance, and impairing receptor recognition. AGEs may also activate specific receptors, like the receptor for AGEs (RAGE), which is present on the surface of all cells relevant to atherosclerotic processes, triggering oxidative stress, inflammation and apoptosis. Understanding the pathogenic mechanisms of AGEs is paramount to develop strategies against diabetic and cardiovascular complications.
晚期糖基化终末产物（AGEs）生成和蓄积的增加与糖尿病相关的大血管和微血管并发症风险升高有关。AGEs是还原糖与蛋白质、脂质和核酸发生非酶促反应的产物，可能通过破坏分子构象、促进交联、改变酶活性、减少其清除以及损害受体识别来改变它们的功能。AGEs还可能激活特定受体，如存在于所有与动脉粥样硬化过程相关细胞表面的AGEs受体（RAGE），引发氧化应激、炎症和细胞凋亡。了解AGEs的致病机制对于制定针对糖尿病和心血管并发症的策略至关重要。
