| Project/Area Number |
16K19388
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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 | The University of Tokyo |
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Principal Investigator |
Maki Hisataka 東京大学, 医学部附属病院, 助教 (00748147)
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| Co-Investigator(Renkei-kenkyūsha) |
Takeda Norihiko 東京大学, 医学部附属病院, 特任講師 (40422307)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | heart failure / pulmonary hypertension / 肺高血圧 / 右心室 / 心臓リモデリング / 内科 |
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| Outline of Final Research Achievements |
Adenosine Tripohsphate (ATP) is consumed in a cardiomyocyte during its contraction process. Elevation of pulmonary artery pressure seemingly increases the ATP demand in the right ventricle. We now have a hypothesis that a mismatch between ATP demand and its production takes places in the hypertrophied heart of right ventricle, leading to a development of right ventricular failure. In this study, we evaluated oxygen consumption and ATP production in right or left ventricular cardiomyocytes and found that ATP synthesis is significantly decreased in right ventricle compared with that in left ventricle. We also mice performed pulmonary artery banding (PAB) and established an in vivo model of right ventricular hypertrophy and heart failure, which we believe will be useful in studying the pathological processes of right ventricular heart failure.
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