2013 Fiscal Year Final Research Report
Tlanslating podocyte biology into new therapys and examinations for podocyte injury
| Project/Area Number |
23591201
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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 |
Kidney internal medicine
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| Research Institution | Kyoto University (2013)
Juntendo University (2011-2012) |
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Principal Investigator |
ASANUMA KATSUHIKO 京都大学, 医学(系)研究科(研究院), 准教授 (60449064)
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| Project Period (FY) |
2011 – 2013
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| Keywords | ポドサイト / 腎障害 / ネフローゼ症候群 / スリット膜 / アポトーシス / 慢性腎臓病 |
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| Research Abstract |
Glomerular visceral epithelial cells, also known as podocytes, serve as the final barrier to urinary protein loss. Podocyte injury may cause podocyte detachment, which leads to glomerulosclerosis. In our established model mice, severe podocyte injury induced podocyte loss and apoptosis, and glomeruloscrelosis. Using the mice model, we reported that treatment of 220oxa-calcitriol and Nothc2 agonist antibody suppressed podocyte loss and apoptosis. Furthermore, we reported that the measurement of urinary podocalyxin may be a useful biomarker to determine activity of IgA nephropathy and the effectiveness of corticosteroid treatment to IgA nephropathy.
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