Elucidation of the qualitative regulatory mechanism of skeletal muscle and its application to overcoming sarcopenia

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K19945
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 59020:Sports sciences-related
• Research Institution: Nagoya Institute of Technology
• Principal Investigator: Ato Satoru 名古屋工業大学, 工学(系)研究科(研究院), 特別研究員(ポスドク) (20825731)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 骨格筋 / 老化 / 筋収縮 / Desmin / 筋核

Outline of Final Research Achievements

This study was undertaken to elucidate the mechanisms of skeletal muscle contractile dysfunction associated with aging and to overcome this problem through its application. It is known that Desmin, a muscle-specific intermediate diameter filament, is involved in the retention of skeletal muscle cell nuclei to the cell periphery and in muscle contractile function. Since accumulation of Desmin in skeletal muscle cells occurs with aging and an increase in the number of central nuclei has been observed in skeletal muscle, we hypothesized that the accumulation of Desmin is associated with the loss of muscle contractile function with aging. We overexpressed Desmin in mouse skeletal muscle and examined its effects on skeletal muscle mass and contractile function, and found that accumulation due to forced Desmin expression reduced skeletal muscle mass without affecting muscle contractile function.

Free Research Field

運動生理学

Academic Significance and Societal Importance of the Research Achievements

本研究は老化に伴う骨格筋収縮機能低下の機序解明とその応用による克服を目指した。骨格筋の中間径フィラメントDesminは骨格筋細胞核の細胞周囲への保持や筋収縮機能に関わっていることが知られている。骨格筋細胞では老化に伴い筋内へDesminの蓄積が生じることや、核が異常な局在を示すことから、Desminの蓄積が筋収縮機能低下と関連する可能性が考えられた。我々はマウス骨格筋へDesminの過剰発現を行い、骨格筋量と筋収縮機能に及ぼす影響の検討を行いDesminの蓄積が筋収縮機能に影響を及ぼさないものの、骨格筋量を低下させる因子であることを明らかにした。