Elucidating molecular mechanisms that control muscle plasticity for healthy longevity

• Project/Area Number: 18H03193
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 59040:Nutrition science and health science-related
• Research Institution: Kumamoto University (2019-2020); Nagasaki University (2018)
• Principal Investigator: Ono Yusuke 熊本大学, 発生医学研究所, 准教授 (60601119)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Project Status: Completed (Fiscal Year 2020)
• Budget Amount: ¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000); Fiscal Year 2020: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000); Fiscal Year 2019: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000); Fiscal Year 2018: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
• Keywords: 筋可塑性 / 筋萎縮 / 筋肥大 / サルコペニア / 加齢 / 骨格筋 / エイジング / 可塑性 / 筋適応

Outline of Final Research Achievements

The average life expectancy in Japan raises, whereas there is a big gap between the life span and “healthy” life span. Age-related sarcopenia is known to be associated with decreasing physical activity and healthy life span. Skeletal muscle plasticity is impaired with aging: Muscle hypertrophic response to overload training is markedly attenuated in the elderly compared with that of young. The mechanism of reduced muscle hypertrophic response is largely unknown but it may relate to the susceptibility to sarcopenia. In this study, we showed that the expression levels of the cell polarity protein Scrib are decreased in muscle of aged mice, which involved in a decline in hypertrophic response to overloading stimulation.

Academic Significance and Societal Importance of the Research Achievements

本研究から，骨格筋における細胞極性因子Scribの発現低下は，加齢にともなう筋可塑性低下の分子基盤になる可能性が示された。Scribは筋肥大応答に必要であり，骨格筋のScrib発現量を保持することは，生涯を通して筋量を維持する上で重要であると考えられる。本成果は，将来，健康寿命延伸に向けたサルコペニア予防改善において，新たな運動・栄養介入の確立や創薬開発への応用が期待できる。