| Project/Area Number |
17K09581
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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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| Research Field |
Cardiovascular medicine
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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)
井手 友美 九州大学, 医学研究院, 准教授 (90380625)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 心不全 / ミトコンドリア / 蛋白取込 / 酸化ストレス / 心筋リモデリング / 循環器・高血圧 |
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| Outline of Final Research Achievements |
In this study, we iaimded to eludicate the role of Tom/Tim complex in cardiac remodeling. In post-infarted hearts, Tim44 protein levels were decreased. Overexpression of Tim44 attenuated left ventricular dilatation and dysfunction, increaseed mitochondiral SOD, and decreased protein carbonylation. In contray, Tim44 knokout demonstrated the opposite effects. These data indictate that Tim44 play a protective role in cardiac remodeling by incraseding import of SOD into mitochondia.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により心筋リモデリングの病態理解が進むのみならず、ミトコンドリア取り込み機能の役割が明らかになり、新たな心不全治療戦略に発展する可能性を有している。
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