Presented in part at the 29th Annual Meeting of the Japanese Society for Apheresis held November 21–23, 2008, in Hiroshima, Japan.
Advanced Glycation End Products and Receptor–Oxidative Stress System in Diabetic Vascular Complications
Version of Record online: 26 NOV 2009
© 2009 The Author. Journal compilation © 2009 International Society for Apheresis
Therapeutic Apheresis and Dialysis
Volume 13, Issue 6, pages 534–539, December 2009
How to Cite
Yamagishi, S.-i. (2009), Advanced Glycation End Products and Receptor–Oxidative Stress System in Diabetic Vascular Complications. Therapeutic Apheresis and Dialysis, 13: 534–539. doi: 10.1111/j.1744-9987.2009.00775.x
- Issue online: 26 NOV 2009
- Version of Record online: 26 NOV 2009
- Received February 2009.
- Advanced glycation end product;
- Advanced glycation end product receptor;
- Diabetic vascular complications;
- Oxidative stress
Reducing sugars can react non-enzymatically with amino groups of protein to form Amadori products. These early glycation products undergo further complex reactions, such as rearrangement, dehydration, and condensation, to become irreversibly cross-linked, heterogeneous fluorescent derivatives, termed advanced glycation end products (AGEs). The formation and accumulation of AGEs have been known to progress at an accelerated rate in patients with diabetes mellitus, thus being involved in the development and progression of diabetic micro- and macroangiopathy. Indeed, there is accumulating evidence that an interaction between an AGE and its receptor (RAGE) generates oxidative stress and subsequently evokes vascular inflammation and thrombosis, thereby playing a central role in diabetic vascular complications. In this paper, we review the pathophysiological role of AGE-RAGE–oxidative stress system and its therapeutic interventions in diabetic micro- and macroangiopathy.