Comprehensive analysis of the mechanism linking between atrial remodeling and stretch or inflammation in atrium.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461045
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Sasano Tetsuo 東京医科歯科大学, 保健衛生学研究科, 准教授 (00466898)
• Co-Investigator(Renkei-kenkyūsha): FURUKAWA TETSUSHI 東京医科歯科大学, 難治疾患研究所, 教授 (80251552)
• Project Period (FY): 2013-04-01 – 2016-03-31
• 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

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.

Free Research Field

不整脈