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晚期糖基化终末产物与受体(RAGE):衰老、糖尿病、神经退行性变及炎症中的共同线索

Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation.

作者信息

Ramasamy Ravichandran, Vannucci Susan J, Yan Shirley Shi Du, Herold Kevan, Yan Shi Fang, Schmidt Ann Marie

机构信息

Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA.

出版信息

Glycobiology. 2005 Jul;15(7):16R-28R. doi: 10.1093/glycob/cwi053. Epub 2005 Mar 10.

Abstract

The products of nonenzymatic glycation and oxidation of proteins and lipids, the advanced glycation end products (AGEs), accumulate in a wide variety of environments. AGEs may be generated rapidly or over long times stimulated by a range of distinct triggering mechanisms, thereby accounting for their roles in multiple settings and disease states. A critical property of AGEs is their ability to activate receptor for advanced glycation end products (RAGE), a signal transduction receptor of the immunoglobulin superfamily. It is our hypothesis that due to such interaction, AGEs impart a potent impact in tissues, stimulating processes linked to inflammation and its consequences. We hypothesize that AGEs cause perturbation in a diverse group of diseases, such as diabetes, inflammation, neurodegeneration, and aging. Thus, we propose that targeting this pathway may represent a logical step in the prevention/treatment of the sequelae of these disorders.

摘要

蛋白质和脂质的非酶糖基化及氧化产物,即晚期糖基化终末产物(AGEs),在多种环境中都会蓄积。AGEs可能会通过一系列不同的触发机制被快速生成,也可能经过很长时间才生成,这就解释了它们在多种情形和疾病状态中所起的作用。AGEs的一个关键特性是它们能够激活晚期糖基化终末产物受体(RAGE),这是一种免疫球蛋白超家族的信号转导受体。我们的假设是,由于这种相互作用,AGEs会对组织产生强大影响,刺激与炎症及其后果相关的过程。我们推测AGEs会在多种疾病中造成紊乱,如糖尿病、炎症、神经退行性变和衰老。因此,我们提出针对这一途径可能是预防/治疗这些疾病后遗症的合理举措。

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