| Project/Area Number |
15K10219
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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 surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大石 恭久 九州大学, 大学病院, 助教 (20529870)
藤本 智子 九州大学, 大学病院, その他(移行) (40567377)
牛島 智基 九州大学, 大学病院, 助教 (70529875)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 心不全 / 心筋疾患 / サルコメア / 分子生物学 / 心筋疾患外科学 / Fhod3 |
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| Outline of Final Research Achievements |
At the embryonic stage, Fhod3 is crucial of cardiac development and achievement of myofibril maturation. The cardiac-specific deletion of Fhod3 in the perinatal stage leads to neonatal lethality, indicating that Fhod3 is essential to myocardial maturation in the normally developed heart.
On the other hand, its specific deletion in the adult heart does not significantly affect the survival. Moreover, the biological response for systemic stimulation with the α1-adrenergic receptor agonist increases more in adult Fhod3-deleted mice, indicating that Fhod3 is associated with functional maintenance of the adult heart.
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