Novel mechanism of progression of diabetic nephropathy by hyperlipidemia: MRP8/TLR4 signaling

高脂血症导致糖尿病肾病进展的新机制：MRP8/TLR4信号传导

• 批准号: 23790939
• 负责人: KUWABARA Takashige
• 金额: $ 2.75万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23790939/
• 关键词: 糖尿病性腎症; 自然炎症; TLR4; MRP8; マクロファージ; 脂質代謝異常

Homeostatic inflammation which is induced by endogenous ligands and pathogenic receptors has been emerged as a molecular basis of life style-related diseases. In this study, it has been clarified that MRP8/TLR4 signaling, involved in homeostatic inflammation, might play an important role in the progression of diabetic nephropathy. Furthermore, renal MRP8 expression in human biopsy samples could predict the renal prognosis of diabetic nephropathy. Blockade of MRP8/TLR4 signaling could become a novel strategy for diabetic nephropathy.

内源性配体和致病性受体诱导的稳态炎症已成为生活方式相关疾病的分子基础。本研究明确了参与稳态炎症的MRP8/TLR4信号通路可能在糖尿病肾病的进展中发挥重要作用。此外，肾MRP8在人体活检样本中的表达可以预测糖尿病肾病的肾脏预后。阻断MRP8/TLR4信号可能成为治疗糖尿病肾病的新策略。

项目成果

糖尿病性腎症における自然炎症の意義とその分子機序

自然炎症在糖尿病肾病中的意义及其分子机制

• 发表时间: 2013
• 作者: Kodama F;Asanuma K;Takagi M;Hidaka T;Asanuma E;Fukuda H;Seki T;Takeda Y;Hosoe-Nagai Y;Asao R;Horikoshi S;Tomino Y;Asanuma K;島村芳子，濱田佳寿，緒方巧二，井上紘輔，香川 亨，井上 眞理，石原正行，高尾 俊弘，渡辺弥夏，湯浅健司，寺田典生;桑原孝成
• 通讯作者: 桑原孝成

Toll-Like Recepotor 4-Mediated, Hyperinsulinemia-Independent Progression of Diabetic Nephropathy by Hyperlipidemia.

Toll 样受体 4 介导的、与高胰岛素血症无关的高脂血症导致的糖尿病肾病进展。

• 发表时间: 2011
• 作者: T Kuwabara;K Mori;M Mukoyama;et al.
• 通讯作者: et al.

Peritoneal Fibrosis and High Transport Are Induced in Mildly Pre-injured Peritoneum by 3,4-Dideoxyglucosone-3-ene in Mice

• DOI: 10.3747/pdi.2011.00033
• 发表时间: 2013-03
• 期刊: Peritoneal Dialysis International
• 影响因子: 2.8
• 作者: H. Yokoi;M. Kasahara;K. Mori;T. Kuwabara;Naohiro Toda;R. Yamada;S. Namoto;Takashi Yamamoto;N. Seki;Nozomi Souma;Takuya Yamaguchi;A. Sugawara;M. Mukoyama;K. Nakao

Annual Review腎臓

年度回顾肾脏

• 发表时间: 2008
• 作者: Matsuzawa A.;et. al.;伊藤恭典
• 通讯作者: 伊藤恭典

京都大学大学院医学研究科内分泌代謝内科

京都大学大学院医学研究科内分泌代谢科