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  1. C. 医薬保健学域; 医学類・薬学類・医薬科学類・保健学類
  2. c 10. 学術雑誌掲載論文(医・保健)
  3. 1. 査読済論文(医学・保健)

Nurture vs. nature in diabetic vasculopathy: roles of advanced glycation endproducts and the receptor for them

https://doi.org/10.24517/00012947
https://doi.org/10.24517/00012947
d948060d-74d0-4db5-a269-5b1f88dcc4c0
名前 / ファイル ライセンス アクション
ME-PR-YAMAMOTO-Y-ICS.1262.164-167.pdf ME-PR-YAMAMOTO-Y-ICS.1262.164-167.pdf (18.0 kB)
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-03
タイトル
タイトル Nurture vs. nature in diabetic vasculopathy: roles of advanced glycation endproducts and the receptor for them
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 10.24517/00012947
ID登録タイプ JaLC
著者 Yamamoto, Yasuhiko

× Yamamoto, Yasuhiko

WEKO 100
e-Rad 20313637
金沢大学研究者情報 20313637
研究者番号 20313637

Yamamoto, Yasuhiko

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Yonekura, Hideto

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e-Rad 80240373
研究者番号 80240373

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Sakurai, Shigeru

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研究者番号 60332665

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Tanaka, Nobushige

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Hui, Li

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Hui, Li

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Khin-Mar, Myint

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Chul-Hee, Kim

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Harashima, Ai

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Osawa, Mari

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Osawa, Mari

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Takeuchi, Masayoshi

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Takeuchi, Masayoshi

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Watanabe, Takuo

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研究者番号 40303268

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Yamamoto, Hiroshi

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研究者番号 00115198

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著者別表示 山本, 靖彦

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山本, 靖彦

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米倉, 秀人

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米倉, 秀人

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原島, 愛

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原島, 愛

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大澤, 真里

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大澤, 真里

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竹内, 正義

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竹内, 正義

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渡邉, 琢夫

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渡邉, 琢夫

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山本, 博

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提供者所属
内容記述タイプ Other
内容記述 金沢大学大学院医学部医学系研究科
書誌情報 International Congress Series

巻 1262, p. 164-167, 発行日 2004-05-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 0531-5131
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1016/j.ics.2003.12.035
出版者
出版者 Elsevier
抄録
内容記述タイプ Abstract
内容記述 As is diabetes itself, diabetic vasculopathy is a multifactor disease. Studies conducted in this lab revealed advanced glycation endproducts (AGE) as the major environmental account for vascular cell derangement characteristic of diabetes, and the receptor for AGE (RAGE) as the major genetic factor that responds to them. AGE fractions that caused the vascular derangement were proven to be RAGE ligands. When made diabetic, 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. They showed marked amelioration of diabetic nephropathy. Extracellular signals and nuclear factors that induce the transcription of human RAGE gene were also identified, which would be regarded as risk factors of diabetic complications. Through an analysis of vascular polysomal poly(A)+ RNA, we came across a novel splice variant coding for a soluble RAGE protein, and named it endogenous secretory RAGE (esRAGE). esRAGE was able to capture AGE ligands and neutralize the AGE action on endothelial cells, suggesting that this variant has a potential to protect blood vessels from diabetes-induced injury. The AGE–RAGE system should thus be regarded as a candidate molecular target for overcoming this life- and quality of life (QOL)-threatening disease.
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
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