2023 Fiscal Year Final Research Report
| Project/Area Number |
21K08082
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53020:Cardiology-related
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
筒井 裕之 九州大学, 医学研究院, 教授 (70264017)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | 心不全 / ミトコンドリア / 小胞体 |
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| Outline of Final Research Achievements |
Cardiac hypertrophy was suppressed in a pressure-load-induced remodeling model in myocardial-specific Mitol knockout mice. This antihypertrophic effect was accompanied by suppression of cardiac hypertrophic signaling factors and reduction of markers of oxidative stress. In addition, siRNA knockdown of Mitol in cardiomyocytes suppressed hypertrophy induced by hypertrophic stimuli. Similar anti-cardiac hypertrophic effects and mechanisms were observed with GRP75 inhibitor treatment.
Inhibition of Mitol and GRP75 function reduced mitochondria-endoplasmic reticulum contact, resulting in an antihypertrophic effect.
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| Free Research Field |
循環器内科学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究はオルガネラの連関という観点から新たな心心筋リモデリング・不全の進展機序を明らかにし、心不全病態の理解に寄与する。さらに、ミトコンドリアと小胞体に対する個別の介入ではなくそれらの関係性への介入が心不全の新たな治療ターゲットとなりうることを示しており、今までにない心不全治療創出の基盤となる。高齢化により心不全パンデミックとして今後増加が予想されている心不全患者に対する医療への貢献が期待される。
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