| Project/Area Number |
16K09651
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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 | Wakayama Medical University |
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Principal Investigator |
Mima Toru 和歌山県立医科大学, 医学部, 准教授 (30373517)
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| Co-Investigator(Kenkyū-buntansha) |
重松 隆 和歌山県立医科大学, 医学部, 教授 (30187348)
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| Research Collaborator |
Yashiro Mitsuru
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | FGF23 / Klotho / エリスロポエチン / B細胞 / ADAM17 / 腎尿細管細胞 / 線維芽細胞増殖因子23 / 相互作用 / ＦＧＦ２３ / Ｋｌｏｔｈｏ / Ｂ細胞 |
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| Outline of Final Research Achievements |
It has been that FGF23 has played an important role in Ca-P metabolism. Newly, We found that FGF23 were crosstalk with erythropoietin in renal epitherial cells. Moreover, number of Klotho positive B cells was decrease in patients with hemodialysis. This may be caused for immunocompromised host of the patients with hemodialysis. We found that One of the causes for decrease of Klotho positive B cells was digested by ADAM17, which was activated in the patients with hemodialysis.
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| Academic Significance and Societal Importance of the Research Achievements |
FGF23とエリスロポエチンは腎不全病態において重要な役割を果たしている。その両者が腎尿細管細胞で相互作用していることは、新たな治療法の開発や創薬のシーズとなる。さらに、B細胞に発現するKlothoの低下が透析患者の易感染性に結び付く可能性は、透析患者の死因の多くを占める感染症について新たな治療法や創薬のシーズとなり医学的意義は大きいい。これらを基に、透析患者の易感染性を完全できれば感染症に費やす医療費の削減も期待でき社会的にも意義は大きい。
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