Novel anti-muscle atrophy signaling via the stress response molecule HO-1

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K19639
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 59040:Nutrition science and health science-related
• Research Institution: The University of Tokushima
• Principal Investigator: UCHIDA Takayuki 徳島大学, 大学院医歯薬学研究部(医学域), 講師 (00803561)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 筋萎縮 / 鉄代謝 / ミトコンドリア

Outline of Final Research Achievements

To maintain skeletal muscle mass, the relationship between iron metabolism and mitochondrial metabolism is crucial. Previous studies have demonstrated that iron deficiency leads to mitochondrial dysfunction and abnormalities in muscle cells. In this study, we investigated how fluctuations in iron levels affect muscle cell metabolism. The results revealed that treatment with the iron chelator DFO resulted in a decrease in mitochondrial proteins and an imbalance in protein synthesis in muscle cells, leading to reduced muscle function. Furthermore, in a muscle atrophy model, it was observed that changes in iron levels affected the expression of muscle atrophy-related genes. These findings suggest that the interplay between iron metabolism and mitochondrial metabolism in muscle cells may contribute to the development of muscle atrophy.

Free Research Field

栄養学および健康科学関連

Academic Significance and Societal Importance of the Research Achievements

本研究を通して、鉄・エネルギー代謝異常から筋萎縮へと繋がる新規経路が明らかになり、大きな学術的意義を持つ。さらに、萎縮環境における鉄付加で筋萎縮抑制傾向がみられたことは、寝たきり状態や消耗性疾患等による筋萎縮を予防するために、食事やサプリメントとしての鉄付加が有効である可能性を示唆しており、社会的意義も大きい。