| Project/Area Number |
25893005
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
SHOUJI Matsushima 北海道大学, 医学(系)研究科(研究院), 助教 (80552869)
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| Co-Investigator(Renkei-kenkyūsha) |
TSUTSUI Hiroyuki 北海道大学, 大学院医学研究科, 教授 (70264017)
KINUKAWA Shintaro 北海道大学, 大学院医学研究科, 講師 (60399871)
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| Research Collaborator |
MATSUMOTO Junichi 北海道大学, 大学院医学研究科
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 心不全 / 心筋リモデリング / ミトコンドリア / 酸化ストレス / NADPH oxidase |
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| Outline of Final Research Achievements |
Cardiomyocyte hypertrophy, interstitial fibrosis, and apoptosis in the non-infarct region of the hearts in mice after myocardial infarction (MI) were increased, which accompanied by a decreae in size of mitochondria and an incrase in number of mitochondria. Protein level of mitofusin 1 was tended to be incrased in non-infarct region of MI mouse hearts compared to sham-operated mouse hearts. In addition, phosphorylation of Drp-1, inhibitory form of Drp-1, was increased in non-infarct region of MI mouse hearts.
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