Homeostatic changes in muscle satellite cells and involvement of Nrf2 / autophagy system in age-related myopathy

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K01487
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Rehabilitation science/Welfare engineering
• Research Institution: Kindai University
• Principal Investigator: Itokazu Maki 近畿大学, 大学病院, 助教 (90780015)
• Co-Investigator(Kenkyū-buntansha): 寺村 岳士 近畿大学, 大学病院, 講師 (40460901) ; 福田 寛二 近畿大学, 医学部, 教授 (50201744)
• Project Period (FY): 2018-02-28 – 2021-03-31
• Keywords: サルコペニア / 筋衛星細胞 / Nrf2 / miRNA-155

Outline of Final Research Achievements

In this study, we focused on muscle satellite cells in order to elucidate the breakdown of tissue homeostasis in "sarcopenia," which is age-related muscle decline. We have been studying the relationship between the antioxidant master gene Nrf2, reactive oxygen species, aging-decreased autophagy, and muscle　homeostasis.
It was found that decreased expression of Nrf2 increased the expression of miRNA-155, which is involved in inflammation and cell aging. Regarding the relationship between miRNA-155 and autophagy, we found that miRNA-155 is involved in the inhibition of mitochondrial selective autophagy in the myoblast cell line C2C12. From the above, we obtained research results that age-related muscle decline is caused by the multifaceted action of miRNA-155.

Free Research Field

リハビリテーション

Academic Significance and Societal Importance of the Research Achievements

サルコペニアは、高齢者におけるQOLの低下の主因とされるが、加齢性筋減衰の機序は未だほとんどが解明されておらず、有効な予防的介入方法は少ない。
本研究では、加齢に伴う筋組織恒常性の破綻を解明するために、筋衛星細胞に注目し研究を行った。加齢性の筋減退はmiRNA-155の多面的な作用により惹起されるという研究成果を得ることができた。これら成果によりmiRNA-155の制御によるサルコペニアの予防や回復の可能性が示唆された。