| Project/Area Number |
16K16430
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
Saito Yuki 札幌医科大学, 医学部, 研究員 (40758702)
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| Research Collaborator |
Chikenji Takako
Fujimiya Mineko
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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 |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 骨格筋 / 再生 / 線維化 / 運動 / 間葉系細胞 / 細胞老化 / 間葉系前駆細胞 / 間葉型前駆細胞 / 骨格筋再生 / 筋炎 / 筋再生 / 理学療法学 / 多発性筋炎 / 運動療法 / リハビリテーション |
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| Outline of Final Research Achievements |
Exercise-induced damage triggers muscle regeneration by activating satellite cells, fibro-adipogenic progenitors (FAPs), and immune cells. FAPs facilitated by exercise play roles for muscle remodeling. On the other hand, in the pathological conditions such as chronic inflammatory myopathy (CIM), exercise-induced damage rather exacerbates the inflammation and fibrosis in the muscle. Although it is considered that FAPs are key regulator for muscle inflammation and fibrosis, the cellular mechanisms are not completely understood.
Here we aimed to demonstrate the mechanism for different roles of exercise-induced damage between normal and CIM by focusing on cell senescence in FAPs. we found that both of sufficient senescence and up-regulation of p38 MAPK, a pro-apoptotic signal, might be necessary for exercise-induced muscle regeneration. On the other hand, insufficient senescence and up-regulation of NF-ΚB, a anti-apoptotic signal might cause exercise-induced inflammation and fibrosis.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性的な炎症を伴う骨格筋疾患は、著明な筋力低下のため、日常生活を著しく困難とさせる。障害された筋機能を回復させるため、運動療法は最も有効な治療法の一つであるが、過剰な運動は炎症を助長したり筋機能を悪化させるリスクも有している。
本研究では、慢性慢性的な炎症を伴う骨格筋障害を呈する動物モデルを使用し、なぜ、運動による筋再生メカニズムと炎症を助長させるメカニズムを解明した。
本研究成果は慢性的な炎症を伴う骨格筋疾患に対する有効で、安全な運動療法を処方するための、基礎的データとなりうる。
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