Elucidation of egulatory mechanism of bone metabolism by lysine deacylase SIRT7.
| Project/Area Number |
17K11014
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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 |
Orthopaedic surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
Yoshizawa Tatsuya 熊本大学, 大学院生命科学研究部(医), 准教授 (40313530)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 骨組織 / 骨粗鬆症 / サーチュイン / SIRT7 / 老化 / ロコモティブシンドローム / アシル化 / 骨芽細胞 / Osterix / 骨代謝 |
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| Outline of Final Research Achievements |
We discovered that the SIRT7, which is the member of Sirtuins (SIRT1-7 in mammals) regulating a wide variety of biological process, is important for bone formation, and have succeeded in finding a new mechanism which activates functions of Osterix transcription factor essential for bone formation. Furthermore, we found that SIRT7 in bone decreased with age. It is expected that the “SIRT7-regulated Osterix activating pathway” will be a new therapeutic drug target to treat decreased osteogenesis and osteoporosis.
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| Academic Significance and Societal Importance of the Research Achievements |
骨粗鬆症では骨吸収を抑える薬剤に比べて骨形成を促進させる薬剤は限られており、骨を再生させる治療薬の開発が望まれている。我々の研究結果によると、老化した場合など SIRT7 が十分に働かない状況では、Osterix の働きが低いために骨を作ることが損なわれ、骨形成低下に伴う骨粗鬆症が引き起こされると考えられた。今後、SIRT7-Osterix の調節経路が骨形成低下に伴う骨粗鬆症の新たな治療薬開発のための標的となることが期待される。
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Report
(3 results)
Research Products
(7 results)
