Involvement of ischemic condition in the pathophysiology of renal damages in obesity-induced kidney injury
Project/Area Number |
26860645
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Kidney internal medicine
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Research Institution | Keio University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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Keywords | 肥満関連腎症 / 慢性腎障害 / 腎虚血 / peritubular capillary / PHD2 / 肥満 / 組織低酸素 / 慢性腎臓病 / 虚血 |
Outline of Final Research Achievements |
Backgrounds: We have reported hypertrophic proximal tubules in obese mice which implies an inefficient oxygen supply in this area (Obesity Int, 2012). We examined whether hypoxic condition in proximal tubules are involved the pathogenesis of obesity-induced renal injury. We also test the hypothesis that this injury can be ameliorated by molecular intervention of prolyl hydroxylase domains (PHDs), sensors for tissue oxygen levels that is a crucial molecule for tissue response to hypoxia. Conclusions: Hypoxic condition due to enlarged cell with vascular rarefaction is evident in the proximal tubular area of obese mice whereas tissue reaction to hypoxic damages failed to properly compensate. The early reduction of PHD2 specifically in the proximal area may constitute a novel strategy against the progression process from an early stage of obesity-induced kidney injury.
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Report
(3 results)
Research Products
(6 results)