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Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice
https://doi.org/10.24517/00013359
https://doi.org/10.24517/000133598d9c1b53-a7fd-44a6-9d56-b3c646dca4f6
名前 / ファイル | ライセンス | アクション |
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ME-PR-YAMAMOTO-H-261.pdf (2.0 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-03 | |||||
タイトル | ||||||
タイトル | Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00013359 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Yamamoto, Yasuhiko
× Yamamoto, Yasuhiko× Kato, Ichiro× Doi, Toshio× Yonekura, Hideto× Ohashi, Seiji× Takeuchi, Masayoshi× Watanabe, Takuo× Yamagishi, Shoichi× Sakurai, Shigeru× Takasawa, Shin× Okamoto, Hiroshi× Yamamoto, Hiroshi |
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著者別表示 |
山本, 靖彦
× 山本, 靖彦× 米倉, 秀人× 渡邉, 琢夫× 櫻井, 繁× 岡本, 宏× 山本, 博 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
Journal of Clinical Investigation 巻 108, 号 2, p. 261-268, 発行日 2001-01-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-9738 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00695520 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1172/JCI200111771 | |||||
出版者 | ||||||
出版者 | American Society for Clinical Investigation | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Vascular complications arising from multiple environmental and genetic factors are responsible for many of the disabilities and short life expectancy associated with diabetes mellitus. Here we provide the first direct in vivo evidence that interactions between advanced glycation end products (AGEs; nonenzymatically glycosylated protein derivatives formed during prolonged hyperglycemic exposure) and their receptor, RAGE, lead to diabetic vascular derangement. We created transgenic mice that overexpress human RAGE in vascular cells and crossbred them with another transgenic line that develops insulin-dependent diabetes shortly after birth. The resultant double transgenic mice exhibited increased hemoglobin A1c and serum AGE levels, as did the diabetic controls. The double transgenic mice demonstrated enlargement of the kidney, glomerular hypertrophy, increased albuminuria, mesangial expansion, advanced glomerulosclerosis, and increased serum creatinine compared with diabetic littermates lacking the RAGE transgene. To our knowledge, the development of this double transgenic mouse provides the first animal model that exhibits the renal changes seen in humans. Furthermore, the phenotypes of advanced diabetic nephropathy were prevented by administering an AGE inhibitor, (±)-2-isopropylidenehydrazono-4-oxo-thiazolidin-5-ylacetanilide (OPB-9195), thus establishing the AGE-RAGE system as a promising target for overcoming this aspect of diabetic pathogenesis. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
関連URI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | http://dx.doi.org/10.1172/JCI200111771 |