| Project/Area Number |
15K19358
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Kyushu University (2016)
Hokkaido University (2015) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TSUTSUI Hiroyuki 九州大学, 大学院医学研究院・循環器内科学, 教授 (70264017)
KINUKAWA Shintaro 北海道大学, 大学院医学研究科・循環病態内科学, 講師 (60399871)
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| Research Collaborator |
MATSUMOTO Junichi 北海道大学, 大学院医学研究科・循環病態内科学, 大学院生
OKABE Kosuke 九州大学, 大学院医学研究院・循環器内科学, 大学院生
IKEDA Soichiro 九州大学, 大学院医学研究院・循環器内科学, 大学院生
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 心筋リモデリング / 心不全 / ミトコンドリア / 酸化ストレス |
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| Outline of Final Research Achievements |
In failing myocardium, mitochondrial size was decreased and number of mitochondria was incraesed. These changes were accompanited by a decrease in phosphorylation of Drp1, a inhibitor form of Drp1, and an increase in Mitofusin1. Treatment with angioteisinII (AngII) increased active form of Drp1 in cardiomyoctyes. GKT137831, a inhibitor of Nox4, inhibited AngII-induced activation of Drp1. These results suggest that Nox4 is a regulator of Drp1 and involved in mitochondrial dynamics in cardiomyocytes.
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