Receptor for advanced glycation end products is a promising target of diabetic nephropathy

Yasuhiko Yamamoto, Toshio Doi, Ichiro Kato, Harumichi Shinohara, Shigeru Sakurai, Hideto Yonekura, Takuo Watanabe, Kihn Mar Myint, Ai Harashima, Masayoshi Takeuchi, Shin Takasawa, Hiroshi Okamoto, Noriyoshi Hashimoto, Masahide Asano, Hiroshi Yamamoto

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)


Advanced glycation end products (AGEs) and the receptor for AGE (RAGE) interactions have been implicated in the development of diabetic vascular complications, which cause various disabilities and shortened life expectancy, and reduced quality of life in patients with diabetes. Diabetes-induced RAGE-overexpressing transgenic mice exhibited the exacerbation of the indices of nephropathy, and this was prevented by the inhibition of AGE formation. We also created RAGE-deficient mice by homologous recombination. They showed marked amelioration of diabetic nephropathy as compared with wild-type mice. Through an analysis of vascular polysomal poly(A)+ RNA, we identified a novel splice variant coding for a soluble RAGE protein and named it endogenous secretory RAGE (esRAGE). esRAGE was able to protect AGE-induced vascular cell injuries as a decoy receptor and was actually detected in human circulation. We conclude that RAGE plays an active role in the development of diabetic vascular complications, especially nephropathy, and is a promising target for overcoming this disease. The esRAGE, an endogenous decoy receptor, may be related to individual variations in resistance to the development of diabetic vascular complications.

Original languageEnglish
Pages (from-to)562-566
Number of pages5
JournalAnnals of the New York Academy of Sciences
Publication statusPublished - 2005


  • AGE
  • Diabetic nephropathy
  • RAGE
  • esRAGE


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