Elucidation of muscular atrophy mechanism by optogenetics oxidative stress induction method and search for therapeutic agents

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K06029
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 42040:Laboratory animal science-related
• Research Institution: Kyoto University
• Principal Investigator: Sato Fuminori 京都大学, ウイルス・再生医科学研究所, 特定助教 (10588263)
• Co-Investigator(Kenkyū-buntansha): 瀬原 淳子 京都大学, ウイルス・再生医科学研究所, 連携教授 (60209038)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: ゼブラフィッシュ / 骨格筋 / 筋萎縮 / 酸化ストレス / ミトコンドリア / オプトジェネティクス

Outline of Final Research Achievements

The purpose of this study is to analyze the process and mechanism by which oxidative stress in skeletal muscle leads to muscular atrophy. Therefore, it is essential to investigate how mitochondrial disorders (overproduction of ROS) in skeletal muscle affect skeletal muscle while maintaining a complex system using Individual organism, and analyze the muscular atrophy process caused.
An attempt was made to establish the above experimental system using zebrafish, but it was not possible to establish a transgenic zebrafish line that expresses a protein that produces ROS by light irradiation in skeletal muscle mitochondria. In order to carry out the research, it is necessary to introduce an expression control system that can control expression control more strictly and to establish a transgenic zebrafish strain again.

Free Research Field

発生生物学

Academic Significance and Societal Importance of the Research Achievements

酸化ストレスによる骨格筋萎縮を生体内のミトコンドリア特異的なROS産生誘導により解析した研究はこれまでほとんどなく、さらにROS産生の誘導方法として光照射を用い、実験対象動物としてゼブラフィッシュを用いたものはない。
新たな骨格筋萎縮機構の解明に貢献するだけでなく、高効率な治療薬スクリーニングなどへの流用も可能である。