A study of molecular mechanisms regulating skeletal muscle mass and strength

2022 Fiscal Year Final Research Report

• Project/Area Number: 21K15369
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 49010:Pathological biochemistry-related
• Research Institution: The University of Tokyo
• Principal Investigator: Eguchi Takahiro 東京大学, 医科学研究所, 助教 (60845056)
• Project Period (FY): 2021-04-01 – 2023-03-31
• 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.

Free Research Field

分子生物学

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。