2021 Fiscal Year Final Research Report
Controlling the aging and metabolic process with anti-stress enzyme expression profiles through those controlling transcriptional factor, Nrf1
| Project/Area Number |
19H04057
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 59040:Nutrition science and health science-related
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
水沼 正樹 広島大学, 統合生命科学研究科(先), 教授 (10343295)
山本 雄広 慶應義塾大学, 医学部(信濃町), 講師 (50383774)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | 老化 / 転写因子 / ポリアミン / 代謝 |
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| Outline of Final Research Achievements |
Increasing reactive oxygen species (ROS) is one of the main cause of aging, and that are detoxifying with the antioxidative proteins that are regulated through group of NF-E2-related factor (Nrf) transcription factors Within this group, Nrf1 has a suppressive function for excessive antioxidant responses and cooperates with Nrf2 to regulate antioxidant mechanisms. To elucidating the molecular mechanisms involved in aging and ROS metabolism, we have been proposed that Nrf1 protein level was changed in the liver of aging mouse model. In this study, comparative analysis of data between Klotho-deficient (Klotho-/-) mice as a model of and aged mice, as well as commonalities with Nrf1-deficient mice, we revealed that polyamine and steroid hormone metabolic pathways are altered during aging. Therefore, we conclude that Nrf1 genes might contribute for aging process.
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| Free Research Field |
生化学
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| Academic Significance and Societal Importance of the Research Achievements |
老化のイベントは多岐にわたり、何が引き金になるのかは不明な点が多い中で、今回Nrf1タンパク質の発現低下が、老化の引き金の一端を担っていることを明確にできた点は大きい。この現象は、マウス個体で得られた成果であることから、ヒトへの外挿可能性も高い。さらにNrf1が制御する代謝経路についても、数種見いだせたので、このタンパク質成分の制御が老化抑制になるのか、今後遺伝子改変動物の作出を通して検証を進め、将来的には、老化を抑制する食品成分や低分子化合物の探索を可能とする情報を提供できた点で学術的に貢献した。
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