Relationship between SGLT1 and ventricular arrhythmia
Project/Area Number |
24590326
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Iwate Medical University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
SANBE Atsushi (30425706)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
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)
|
Keywords | SGLT1 / 心不全 / 高血圧症 / 急性虚血 / 心筋肥大 / 心室性不整脈 / ナトリウムーグルコース共輸送機構1 / ナトリウム-グルコース共輸送機構1 |
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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Report
(4 results)
Research Products
(2 results)