Theraputic strategy for for idiopathic nephrotic syndrome targetted against molecules expressed on podocytes
| Project/Area Number |
25461634
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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 | 微小変化型ネフローゼ症候群 / ポドサイト / エンドセリン / エンドセリン受容体拮抗薬 / アンブリセンタン / 微小変化型ネフローゼ症候 / 微少変化型ネフローゼ症候群 / CD80分子 / PANラット / イグラチモド / 抗リウマチ薬 / lipopolysaccharide |
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| Outline of Final Research Achievements |
The abnormal expression of podocyte-related molecules has been attracting attention with respect to the pathogenesis of minimal change nephrotic syndrome (MCNS). Even in the case of endothelin (ET), which has a potent vasoconstrictor effect, it has become clear that the receptor is expressed in the podocytes, and the possibility of ET causing proteinuria and structural changes in podocytes has been reported. Therefore, the possibility of using ET antagonistic drug was investigated using rat models. According to the results, the proteinuria in the treatment group was lower than the significant proteinuria in the untreated group. Upon electron microscope observation, the characteristic foot process fusion of podocytes was found in the untreated group, but not in the treatment group. The results suggested that the ETA antagonists directly act on podocytes to exhibit an anti-proteinuric effect, and it was thought to have potential as a therapeutic agent for MCNS.
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Report
(4 results)
Research Products
(9 results)
