| Project/Area Number |
23591093
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
ASANUMA HIROSHI 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (20416217)
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| Co-Investigator(Kenkyū-buntansha) |
ASAKURA Masanori 独立行政法人国立循環器病研究センター, 臨床研究企画室, 室長 (80443505)
KITAKAZE Masafumi 独立行政法人国立循環器病研究センター, 臨床研究部, 部長 (20294069)
HIRAIDE Atsushi 近畿大学, 医学部, 教授 (20199037)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 心不全 / トランスレーショナルリサーチ / 循環器内科学 / 分子心臓病態学 / 循環器・高血圧 |
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| Research Abstract |
We examined whether AMPK activation can modulate cardiac remodeling and inhibit the progression of heart failure in the canine myocardial infarction model and pacing induced decompensated heart failure, which is considered to be similar to human dilated cardiomyopathy and can be superimposed on translational study for human heart failure. Neither blood pressure nor heart rate differed between the groups with and without AICAR (AMPK activator) at 6 weeks after the onset of myocardial infarction or pacing-induced heart failure. Left ventricular ejection fraction increased, and mean pulmonary arterial pressure and pulmonary capillary wedge pressure decreased in the AICAR treated group compared with the untreated group. These effects were observed in both models, even after the onset of heart failure. Thus, we conclude that AMPK activation is an important novel therapeutic target in chronic heart failure.
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