Mechanism of skeletal muscle remodeling and regeneration for the prevention of frailty and sarcopenia
| Project/Area Number |
18K15414
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52010:General internal medicine-related
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| Research Institution | Nagoya University |
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Principal Investigator |
Inoue Aiko 名古屋大学, 未来社会創造機構(医), 招へい教員 (10805245)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 骨格筋 / 再生 / リモデリング / 加齢 |
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| Outline of Final Research Achievements |
Skeletal muscle in the elderly is often accompanied with damage (e.g., sarcopenia, frailty, etc.), and the approach to the skeletal muscle regeneration is necessary for the treatment. Notch-1 signaling, which plays an important role in cell differentiation, proliferation, and apoptosis, is reported to be inactivated during aging. Cathepsin K has been reported to activate Notch1. In this study, we have investigated the mechanism of sarcopenia, specially focused on cathepsin K-mediated Notch1 singling activation. We found that cathepsin K is involved in skeletal muscle disorders such as sarcopenia.
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| Academic Significance and Societal Importance of the Research Achievements |
カテプシンKが、カヘキシアモデルマウスの骨格筋の萎縮と機能障害にも関与している可能性が示唆されたことにより、今後は高齢者のQOLやADLの低下予防や、フレイルなどの改善のための新たな分子標的になる可能性が示唆された。
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Report
(4 results)
Research Products
(3 results)
