| Project/Area Number |
25461045
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
Sasano Tetsuo 東京医科歯科大学, 保健衛生学研究科, 准教授 (00466898)
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| Co-Investigator(Renkei-kenkyūsha) |
FURUKAWA TETSUSHI 東京医科歯科大学, 難治疾患研究所, 教授 (80251552)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 心房細動 / 細胞外ATP / マイクロRNA / 高脂肪食 / 糖尿病 / 圧負荷 / メタボリック症候群 / ギャップジャンクション / 心房リモデリング / ATP / 線維化 / 炎症 / 心房圧負荷 / pannexin / 炎症性サイトカイン |
|---|
| Outline of Final Research Achievements |
It has been well known that lifestyle-related diseases like hypertension, metabolic syndrome, and diabetes are the risk of atrial fibrillation. We aimed to clarify the mechanism linking these pathological conditions and atrial arrhythmias using mice model, focusing on the involvement of microRNA (miR). We performed electrophysiological analysis and comprehensive expression analysis of miR, to identify the miRs playing a key role for atrial arrhythmias.
We then performed thorough examination in metabolic syndrome model, and found that the expression of miR-27b was increased in atrium. The expression of Cx40, a major gap-junction channel in atrium was regulated by miR-27b. The increased expression of miR-27b caused the conduction disturbance, resulting in the higher inducibility of atrial tachyarrhythmias.
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