Analysis of the molecular mechanism of immobilization-induced muscle atrophy

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K23998
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0904:Internal medicine of the bio-information integration and related fields
• Research Institution: Kobe University
• Principal Investigator: HIRATA Yu 神戸大学, 医学部附属病院, 医員 (70846352)
• Project Period (FY): 2019-08-30 – 2021-03-31
• Keywords: 骨格筋 / 不動化性筋萎縮 / KLF15

Outline of Final Research Achievements

We have analyzed the molecular mechanism of skeletal muscle atrophy due to immobilization. Transcription factor KLF15 is an important regulator in immobilization-induced muscle atrophy. It was revealed that transcription factor C/EBPβ and δ are involved upstream of KLF15. We have also searched for target factors that function downstream of KLF15, and identified a humoral factor that increased both in mice and human during immobilization. These results suggest that immobilization induces muscle atrophy via a C/EBP-KLF15 axis.

Free Research Field

糖尿病代謝学

Academic Significance and Societal Importance of the Research Achievements

サルコペニアは加齢に伴う筋量減少と身体活動能力の低下に特徴付けられる病態であり、超高齢社会を迎えたわが国における健康寿命短縮の重要な原因である。身体活動の低下や不動化はサルコペニアの発症要因であるが、不動化による筋萎縮のメカニズムは明らかではない。本研究では、不動化性筋萎縮においてC/EBP-KLF15経路が重要な役割を担うことを明らかとした。本研究結果は筋萎縮抑制薬の開発に資する可能性がある。