| Project/Area Number |
25670414
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
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| Co-Investigator(Kenkyū-buntansha) |
KANASAKI Keizo 金沢医科大学, 医学部, 准教授 (60589919)
KANASAKI Megumi 金沢医科大学, 医学部, 助教 (50599355)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | オートファジー / 糖尿病 / 内皮・間葉転化 / microRNA / 内皮細胞 / IL-6 / AcSDKP / 腎線維化 / miRNA / 糖尿病腎症 / マイクロRNA / メトフォルミン |
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| Outline of Final Research Achievements |
Renal fibrosis in diabetic mouse model was ameliorated by inhibition of endothelial-mesenchymal conversion via the anti-fibrotic microRNA29 and let-7 induction with an endogenous anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) administration. In addition, although renal fibrosis has been caused by the enhancement of the DPP-4 expression by reduced microRNA29 expression in diabetic state, it has improved by microRNA29 expression with a DPP-4 inhibitor, linagliptin administration.
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