The effects of load-induced Ca2+ signaling on muscle hypertrophy and sarcopenia

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K24306
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0909:Sports sciences, physical education, health sciences, and related fields
• Research Institution: Foundation for Biomedical Research and Innovation at Kobe
• Principal Investigator: Naoki Ito 公益財団法人神戸医療産業都市推進機構, その他部局等, 研究員(上席・主任研究員クラス) (50746534)
• Project Period (FY): 2019-08-30 – 2021-03-31
• Keywords: 骨格筋 / 筋肥大 / 筋萎縮 / サルコペニア

Outline of Final Research Achievements

Sarcopenia, age-related muscle weakness with decreases in muscle strength and mass, has become a social problem. In particular, sarcopenia has been associated with the reduced protein synthesis in response to exercise and/or protein intake, termed anabolic resistance. In this study, we focused on intracellular Ca2+ signaling and analyzed the molecular mechanisms that connect mechanical load and the increases in muscle mass. Furthermore, under the hypothesis that the disruption of Ca2+ signaling is the cause of anabolic resistance, load-induced and Ca2+ signaling-dependent intramuscular signal transduction was analyzed by comparative analysis of load-dependent and Ca2+ signaling-dependent gene expression.

Free Research Field

骨格筋分子生物学

Academic Significance and Societal Importance of the Research Achievements

アナボリックレジスタンスの原因は大部分が未解明であり、その改善法も確立されていない。その理由として、そもそも、どのようなメカニズムを介して運動または負荷依存的な筋量の増加（タンパク質合成の活性化）が生じるのか、という基本的な問いに対する答えが得られていないことが挙げられる。本研究によって、サルコペニアおよびアナボリックレジスタンスの分子病態の一端が明らかにされることにより、サルコペニアに対する分子標的・創薬技術基盤の構築が期待される。