| Project/Area Number |
15K09078
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
Honjo Haruo 名古屋大学, 環境医学研究所, 准教授 (70262912)
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| Co-Investigator(Kenkyū-buntansha) |
辻 幸臣 長崎大学, 医歯薬学総合研究科(医学系), 講師 (60432217)
山崎 正俊 東京大学, 大学院工学系研究科(工学部), 特任研究員 (30627328)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 不整脈 / ギャップ結合 / 心臓電気生理学 / 活動電位 / イオンチャネル / 心臓電気生理 / 電気生理学 |
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| Outline of Final Research Achievements |
Arrhythmogenic remodeling of myocardial gap junctions was investigated using a transgenic mouse model with cardiac dysfunction/lethal ventricular arrhythmias, and a rabbit electrical storm model induced by sustained severe bradycardia. In diseased hearts, connexin43 expression was decreased in the intercalated disc region of ventricular myocytes, which was associated with a reduction of conduction velocity and an increase in the spatial heterogeneity of action potential repolarization, leading to increased susceptibility of reentrant ventricular tachyarrhythmias. In addition, the results suggested that the renin-angiotensin system and calmodulin/CAMKII are involved in arrhythmogenic gap junction remodeling in diseased hearts.
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