| Project/Area Number |
18K15706
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52050:Embryonic medicine and pediatrics-related
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 川崎病 / モデルマウス / 心筋炎 / 心筋炎モデルマウス / 不整脈 / 血管炎モデルマウス / 川崎病モデルマウス / バイオマーカー |
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| Outline of Final Research Achievements |
We measured cardiac function over time after FK565 administration, cardiac function decreased from 1 week after administration and gradually improved from 3 months after administration. In this model mice, abnormal excitatory regions were observed in the atrium appendage and action potential prolongation was observed. In isolated cardiomyocytes, L-type Ca2+ current was measured using the patch clamp method, and was significantly decreased. The decay time of Ca2+ transient induced by caffeine was increased, suggesting that NCX function was impaired. These results suggested that FK565 treatment decreased L-type Ca2+ current and Ca2+ transient, which downregulated SERCA and NCX, resulting in impaired cardiac function.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、心筋炎によって惹起される致死性不整脈のメカニズムをイオンチャネルレベルで明らかにし、心筋炎時に抗不整脈薬に対する感受性がどのように変化するのかを追求することを目的とし、研究を行った。心筋炎によって惹起される致死的不整脈の背景となる電気生理学的メカニズムは不明な点も多く、小児領域では使用できる薬剤も限られており、本研究により治療法や予防法の考察に貢献できたと考えている。
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