@article{oai:kanazawa-u.repo.nii.ac.jp:00012959,
 author = {山本, 靖彦 and 米倉, 秀人 and 竹内, 正義 and 渡邉, 琢夫 and 櫻井, 繁 and 岡本, 宏 and 山本, 博 and Yamamoto, Yasuhiko and Kato, Ichiro and Doi, Toshio and Yonekura, Hideto and Ohashi, Seiji and Takeuchi, Masayoshi and Watanabe, Takuo and Sakurai, Shigeru and Yasui, Kiyoshi and Ralica, Petrova G and Joynal, Abedin and Hui, Li and A.K.M.Azadur, Rahman and Takasawa, Shin and Okamoto, Hiroshi and Yamamoto, Hiroshi},
 journal = {International Congress Series},
 month = {Nov},
 note = {Vascular complications are what eventually threaten the lives of diabetic patients. Here we show direct in vivo evidence that the interaction between advanced glycation end products (AGE), the formation of which is accelerated during prolonged hyperglycemic exposure, and a cell surface receptor for AGE (RAGE) is the major cause of such complications. We created transgenic mice that overexpress human RAGE in vascular cells and crossbred them with another transgenic line which develops insulin-dependent diabetes early after birth. The resultant double transgenic mice exhibited accelerated kidney changes compared with single transgenic littermates, and the nephropathy was ameliorated by an inhibitor of AGE formation. The AGE–RAGE system will thus be a promising target for overcoming diabetic complications., 金沢大学大学院医学部医学系研究科},
 pages = {45--50},
 title = {The role of AGE-Rage system in the development of diabetic nephropathy in vivo},
 volume = {1245},
 year = {2002}
}