Role of SOD in the pathogenesis of diabetic nephropathy
| Project/Area Number |
20590943
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Akita University |
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Principal Investigator |
FUJITA Hiroki Akita University, 医学部, 講師 (30333933)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Yuichiro 秋田大学, 大学院・医学系研究科, 教授 (60283610)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 糖尿病性腎症 / 酸化ストレス |
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| Research Abstract |
Superoxide dismutase (SOD) is a major anti-oxidant enzyme which scavenges superoxide anion. In the present study, we found that SOD is down-regulated in the kidneys of diabetic mice susceptible to nephropathy, leading to renal superoxide overproduction. Furthermore, we demonstrated that SOD mimetic dramatically prevents the progression of diabetic nephropathy in these mice via reducing renal superoxide production. We conclude that SOD plays an important role in preventing renal damage by oxidative stress inducing under chronic hyperglycemia.
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Report
(4 results)
Research Products
(9 results)
