| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
First, we demonstrated that SGLT1 prevents VT through the inhibition of calcium overload and the improvement of impulse conduction slowing during ischemia. Second, we demonstrated that SGLT1 gene and protein expression was increased chronic pressure overload-induced cardiomyopathy. Moreover, SGLT1 participated in cardiac remodeling such as cardiac hypertrophy, the increased cardiac fibrosis, heart failure observed by the reduction of left ventricular fractional shortening, and ventricular tacyarrhythmia induction in chronic. pressure overload-induced cardiomyopathy. The results suggest that SGLT1 plays important roles in the induction of ischemia-induced VT in acute global ischemia guinea pig model, and cardiac remodeling, and heart failure in pressure overload-induced cardiomyopathy. This study provides new information regarding the possibility of the development of a new anti-arrhythmic and ant-heart failure drugs.
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