2018 Fiscal Year Final Research Report
Elucidation of podocyte-specific TGF-beta suppression mechanism using R3hdml and examination of therapeutic application
Project/Area Number |
16K19530
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Metabolomics
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Research Institution | Chiba University |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | ポドサイト / 糖尿病性腎症 / TGF-β / p38MAPK |
Outline of Final Research Achievements |
The purpose of this study was to elucidate the role of podocyte-specific gene R3hdml in diabetic nephropathy. In studies using cultured podocytes, R3hdml was found to suppress apoptosis of podocytes through suppression of p38 MAPK phosphorylation among MAPKs. In addition, changes in glomerular basement membrane and podocyte foot processes characteristic of diabetic nephropathy were observed in R3hdml knockout mice. In addition, albuminuria increased when diabetes was induced in R3hdml knockout mice. Furthermore, it was revealed that in R3hdml overexpressing mice, albumin excretion in urine is reduced in diabetic state as compared to wild type under the same condition. Thus, R3hdml may be a protective factor in the development of diabetic nephropathy.
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Free Research Field |
糖尿病性腎症
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Academic Significance and Societal Importance of the Research Achievements |
本研究成果は、将来的なR3hdmlを用いたポドサイト特異的な糖尿病性腎症の治療法を確立に繋がる可能性がある。
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