| Project/Area Number |
23K24331
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| Project/Area Number (Other) |
22H03070 (2022-2023)
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Multi-year Fund (2024)
Single-year Grants (2022-2023) |
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| Section | 一般 |
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| Review Section |
Basic Section 53020:Cardiology-related
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| Research Institution | International University of Health and Welfare |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
瀬戸山 大樹 九州大学, 大学病院, 助教 (30550850)
絹川 真太郎 九州大学, 医学研究院, 准教授 (60399871)
松島 将士 九州大学, 医学研究院, 助教 (80552869)
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| Project Period (FY) |
2024-04-01 – 2025-03-31
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| Project Status |
Completed (Fiscal Year 2024)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2024: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2023: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2022: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | 心筋リモデリング / 心不全 / ゴルジ体 / ミトコンドリア / 小胞体 / オルガネラ / オルガネラネットワーク |
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| Outline of Research at the Start |
継続課題のため、記入しない。
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| Outline of Final Research Achievements |
Cyclin-dependent kinase 5 (CDK5) pathway was activated in heart failure models, including post-myocardial infarction, pressure overload-induced hypertrophy, and continuous angiotensin II infusion. CDK5 was involved in the regulation of Golgi apparatus fragmentation in failing cardiomyocytes. Furthermore, suppression of CDK5-mediated Golgi structural abnormalities attenuated the Golgi stress response, as well as endoplasmic reticulum stress, mitochondrial dysfunction, and oxidative stress, leading to reduced cardiac remodeling and improved cardiac function.
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| Academic Significance and Societal Importance of the Research Achievements |
ゴルジ体が、細胞内オルガネラネットワークおよび心筋リモデリング・心不全の形成および進展において重要な役割を果たすことが初めて示された。本研究成果は、オルガネラネットワークの起点となるゴルジ体の制御が、独自のパラダイムに基づく新たな心不全の予防・治療法の開発へと発展する可能性を示唆するものである。
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