| Project/Area Number |
26860651
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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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 |
WATANABE Ai 金沢医科大学, 医学部, 助教 (70625722)
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| Research Collaborator |
KITADA Munehiro 金沢医科大学, 医学部, 准教授 (40434469)
KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 糖尿病腎症 / Sirt3 / ミトコンドリア / 酸化ストレス / CD38 / オートファジー / カロリー制限 / サーチュイン / ﾐﾄｺﾝﾄﾞﾘｱ |
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| Outline of Final Research Achievements |
Mitochondrial (Mt) oxidative stress, which is important for the pathogenesis of diabetic nephropathy, is caused by the breakdown of active oxygen species production / antioxidant balance and Mt function decline / homeostatic maintenance. The NAD + dependent deacetylase (Sirt 3) plays an important role in controlling Mt redox and Mt homeostasis. In renal proximal tubular cells of Zucker Diabetic fatty rats, the increase in NAD + consumption posibly due to the increased expression of CD38, which is known as NAD+ degrading enzyme, and the decrease in Sirt 3 function contributed to the enhancement of Mt oxidative stress。And than, the autophagy function is impaired in the kidney of diabetic rats, resulting in the accumulation of abnormal Mt and the breakdown of Mt homeostasis, which is involved in the initiation and progression of diabetic nephropathy.
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