Advanced glycation end products in diabetes associated atherosclerosis and renal disease - Interventional studies
Advanced glycation end products in diabetes associated atherosclerosis and renal disease - Interventional studies
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DOI：
10.1196/annals.1333.088
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Allen, TJ
中科院分区：
文献类型：
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作者：
Jandeleit-Dahm, KA;Lassila, M;Allen, TJ
越来越多的证据表明，晚期糖基化终产物（AGEs）及其与各种受体（特别是受体β）的相互作用在糖尿病大血管和微血管并发症的发生和发展中起着关键作用。已经使用了几种方法来抑制糖尿病中AGE的组织积累，包括AGE形成的抑制剂如氨基胍、ALT 946和吡哆胺或假定的交联破坏剂如ALT 711。替代的干预措施还包括给予可溶性AGEs受体sAGEs，从而捕获循环AGEs并防止它们与细胞结合的全长受体sAGEs结合，从而抑制AGE-sAGEs结合后的促炎和促纤维化反应。在这篇综述中，我们总结了这种抗糖化治疗在延缓或延缓糖尿病相关动脉粥样硬化和肾脏疾病的发展和进展的证据，同时关注抑制AGE积累的干预策略。总之，所有方法都显示出一定程度的抗动脉粥样硬化和肾保护作用，尽管程度不同，机制不同。
There is increasing evidence that advanced glycation end products (AGEs) and their interactions with various receptors (in particular, the receptor RAGE) play a pivotal role in the development and progression of diabetic macro- and microvascular complications. Several approaches have been used to inhibit tissue accumulation of AGEs in diabetes, including inhibitors of AGE formation such as aminoguanidine, ALT 946, and pyridoxamine or putative cross-link breakers such as ALT 711. Alternative interventions have also included the administration of a soluble receptor for RAGE, sRAGE, thus capturing circulating AGEs and preventing them from binding to the cell-bound full-length receptor RAGE, thereby inhibiting the proinflammatory and profibrotic response following AGE-RAGE binding. In this review we summarize the evidence for such antiglycation therapies in retarding or delaying the development and progression of diabetes-associated atherosclerosis and renal disease while focusing on interventional strategies inhibiting AGE accumulation. In summary, all approaches have been shown to confer some degree of antiatherosclerotic and renoprotective effects, albeit to different degrees and by different mechanisms.