Development of a new treatment for skeletal muscle atrophy by targeting human pseudogene

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K08646
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: Fujita Health University
• Principal Investigator: Hitachi Keisuke 藤田医科大学, 総合医科学研究所, 助教 (10508469)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: タンパク質メチル化修飾 / 骨格筋 / 筋萎縮 / 筋肥大 / メチル化酵素

Outline of Final Research Achievements

By analyzing the skeletal muscle tissue of the knockout mouse of protein methyltransferase Mettl21e, I revealed that Mettl21e is a novel regulator of skeletal muscle mass. I also identified a skeletal muscle protein as a substrate for Mettl21e and found that Mettl21e regulates skeletal muscle mass through the methylation of muscle protein. Although the use of Mettl21e to increase the size of human skeletal muscle cells has not yet been successful due to the issue of gene transfer efficiency, it was suggested that Mettl21e could be applied to new treatments for human muscle atrophy by improving the method.

Free Research Field

医化学一般

Academic Significance and Societal Importance of the Research Achievements

疾患や老化によって引き起こされる骨格筋の量の減少（筋萎縮）は、疾患での生存率やQOL（クオリティ・オブ・ライフ）を低下させるだけでなく、社会的な生産性の低下にもつながる。しかしながら、筋萎縮に対する安全で有効な治療薬は未だ存在しない。本研究により、骨格筋量の制御とタンパク質のメチル化修飾の意義が明らかとなったことで、将来的には特定のタンパク質のメチル化修飾を標的とした筋萎縮に対する新たな創薬が可能になると考えられる。