| Budget Amount *help |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2018: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
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| Outline of Final Research Achievements |
Atrial fibrillation (Af) is a common arrhythmic disorder rapidly increasing in developed countries, and shows complex pathogenesis involving both structural and electrical remodeling that is frequently associated with other cardiac and metabolic/systemic diseases. This study aimed to comprehensively understand how stress-responsive molecules such as TRPM4 and TRPM7 channels can contribute to Af pathogenesis and some conduction disorders as well, by the combination of electrophysiological measurement and numerical simulation. The results, in particular, from cocultured cardiomyocyte/fibroblast monolayers and their equivalent 2D-model-based simulations suggested the critical importance of the synergy between excessive TRPM channel activity and fibroblast activation in promoting the arrhythmogenic processes.
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