2022 Fiscal Year Final Research Report
A study of molecular mechanisms regulating skeletal muscle mass and strength
Project/Area Number |
21K15369
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 49010:Pathological biochemistry-related
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Research Institution | The University of Tokyo |
Principal Investigator |
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Project Period (FY) |
2021-04-01 – 2023-03-31
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Keywords | 骨格筋 / 筋萎縮 / 筋肥大 / CaMKII |
Outline of Final Research Achievements |
Skeletal muscle is required for motor function, and severe muscle atrophy leads to reduced muscle strength. Calcium ion (Ca2+) is essential for skeletal muscle contraction, and plays a key role in regulating the skeletal muscle mass; however, its underlying mechanisms remain unclear. In the present study, we demonstrated that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is involved in the muscle atrophy/hypertrophy, suggesting the importance of CaMKII in developing therapeutics aimed at improving muscle atrophy.
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Free Research Field |
分子生物学
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Academic Significance and Societal Importance of the Research Achievements |
我々の生命活動において骨格筋は必須の役割を担っており、重篤な筋萎縮は筋力・運動機能の低下を引き起こし生活の質(QOL)を低下させる。本研究ではカルシウムイオン(Ca2+)によって活性化されるCa2+/calmodulin-dependent protein kinase II (CaMKII)に着目し、CaMKIIβサブユニット、およびその類縁分子が筋萎縮/筋肥大の関連因子であることを明らかにした。それゆえ、本研究成果は筋萎縮の分子メカニズムの理解を深め、筋萎縮治療技術の基盤開発を促進したといえる。
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