| Project/Area Number |
17K10189
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Sato Masashi 和歌山県立医科大学, 医学部, 客員研究員 (30726716)
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| Co-Investigator(Kenkyū-buntansha) |
中西 浩一 琉球大学, 医学(系)研究科(研究院), 教授 (50336880)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 嚢胞性腎疾患 / cpkマウス / smadリン酸化 / smad3リン酸化 / 多発性嚢胞腎 / Smad3部位特異的リン酸化 |
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| Outline of Final Research Achievements |
Polycystic kidney disease (PKD) is characterized by abnormal proliferation, secretion and fibrosis in the tubules of the kidneys. These cause cyst formation in the tubules and lead to renal failure.It was suggested that one of phosphorylated Smad3, p-SmadL/C, is involved in the cyst formation and enlargement.In viral associated chronic liver disease, it was reported that inhibition of a molecule in the upstream of pSmad3L lead to upregulation of pSmad3C-associated cascade, which is related to normal apoptosis.
Therefore, inhibition of a molecule in the upstream of pSmad3L also may be a therapeutic strategy for inhibition of cyst formation in PKD.
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| Academic Significance and Societal Importance of the Research Achievements |
多発性嚢胞腎は根本的な治療薬の開発がいまだ十分とはいえず、徐々に腎機能が低下し腎不全に至ると腎移植や透析治療となることが避けられない。ウイルス性慢性肝障害や大腸癌などSmad3の関与が研究されているのと同様に、多発性嚢胞腎においてもSmad3のリン酸化部位に着目した治療薬の開発に本研究が大きく貢献する可能性が示された。
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