| Project/Area Number |
23659140
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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 |
General pharmacology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
YABE Chihiro 京都府立医科大学, 大学院・医学研究科, 教授 (70150571)
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| Co-Investigator(Kenkyū-buntansha) |
IWATA Kazumi 京都府立医科大学, 医学研究科, 講師 (60305571)
MSATSUMOTO Misaki 京都府立医科大学, 医学研究科, 助教 (80533926)
CHOU Ka 京都府立医科大学, 医学研究科, プロジェクト研究員 (50599222)
松野 邦晴 京都府立医科大学, 医学(系)研究科(研究院), 助教 (50420708)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 循環器・高血圧 / 不整脈 / チャネル / 活性酸素種 |
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| Research Abstract |
Reactive oxygen species (ROS) have been implicated in the pathogenesis of atrial fibrillation by affecting ion channels of cardiomyocytes. In animal model of sepsis, susceptibility to cardiac arrhythmia is augmented. Since we previously demonstrated that a novel isoform of superoxide-generating NADPH oxidase, NOX1, was up-regulated in septic heart to elicit cardiomyocyte apoptosis, a possible involvement of NOX1 in the development of cardiac arrhythmia was investigated using mice deficient in Nox1.
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