| Budget Amount *help |
¥85,540,000 (Direct Cost: ¥65,800,000、Indirect Cost: ¥19,740,000)
Fiscal Year 2014: ¥13,520,000 (Direct Cost: ¥10,400,000、Indirect Cost: ¥3,120,000)
Fiscal Year 2013: ¥14,170,000 (Direct Cost: ¥10,900,000、Indirect Cost: ¥3,270,000)
Fiscal Year 2012: ¥14,950,000 (Direct Cost: ¥11,500,000、Indirect Cost: ¥3,450,000)
Fiscal Year 2011: ¥14,690,000 (Direct Cost: ¥11,300,000、Indirect Cost: ¥3,390,000)
Fiscal Year 2010: ¥28,210,000 (Direct Cost: ¥21,700,000、Indirect Cost: ¥6,510,000)
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| Outline of Final Research Achievements |
The present study aimed at exploring novel pathogenic mechanisms underlying abnormal excitability and arrhythmic changes in stressed hearts. For this purpose, we focused on stress-responsive Ca2+/Na+ channel molecules transient receptor potential (TRP) proteins, and investigated their pathological significance by combining both experimental and theoretical approaches. The results clearly indicate that post-remodeling upregulation as well as small differences in PIP2 sensitivity among highly homologous isoforms and arrhythmic mutations could account for part of their notably different functionalities, leading to enhanced risk of arrhythmias and abnormal excitability. This integrative approaches of experiments and numerical model-based simulations may provide a useful framework to design/develop new anti-arrhythmic drugs targeting TRP channels and simultaneously facilitate our understanding about an otherwise elusive complexity of cardiac excitation/propagation and its disorders.
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