| Project/Area Number |
25670387
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SHINTANI Norihito 大阪大学, 薬学研究科, 准教授 (10335367)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 心肥大 / ミトコンドリア / 心不全 |
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| Outline of Final Research Achievements |
In cardiomyocytes, mitochondria play central roles in metabolism, energy production and cell death. Mitochondria maintain its homeostasis through continuous fusion and fission process. Mitochondrial inner-membrane fusion inhibitor (MIFI) regulates mitochondrial morphology via inhibiting inner-membrane fusion. Since the expression of MIFI is predominant in heart and decreased after myocardial infarction or pressure overload, we generated transgenic mice with cardiac specific overexpression of MIFI (MIFI-TG) to assess functional roles in cardiac pathophysiology. Overexpression of MIFI were confirmed by enhanced protein expression in heart and transgenic mice were obtained according to Mendelian’s law. While no overt cardiac phenotype was observed under physiological condition, MIFI-TG displayed accelerated cardiac hypertrophy and dysfunction, suggesting mitochondrial morphological changes caused by MIFI are detrimental after stress stimulation in heart.
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