| Project/Area Number |
19500357
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
KURIHARA Satoshi Jikei University School of Medicine, 医学部, 教授 (90057026)
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| Co-Investigator(Kenkyū-buntansha) |
HONGO Kenichi 東京慈恵会医科大学, 医学部, 准教授 (00256447)
KOMUKAI Kimiaki 東京慈恵会医科大学, 医学部, 講師 (60360145)
SASAKI Hiroyuki 東京慈恵会医科大学, 医学部, 准教授 (60170693)
FUKUDA Norio 東京慈恵会医科大学, 医学部, 講師 (30301534)
MORIMOTO Sachio 九州大学, 医学研究科, 准教授 (50202362)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 心筋 / トロポニンT / Ca^<2+>感受性 / アンギオテンシンII受容体 / Ca^<2+> / トロポニン / 細胞内Ca^<2+> / 筋小胞体 / Ca感受性 / 拡張型心筋症 / Caトランジェント / アンギオテンシンII / DCM / マウス / 細胞内Ca / Ca transient / レニン・アンギオテンシン系 / 心エコー / Ca 感受性 / 細胞内Ca2^<2+> / CaMKII |
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| Research Abstract |
We explored the mechanism of pathogenesis and sudden death in dilated cardiomyopathy using knock-in mouse model with mutant troponin T (DCM mouse). DCM mouse died suddenly from age of 1 month old. In DCM mouse, cardiac chamber was dilated and contractile functions were impaired. A blocker of angiotensin II receptor (ARB) significantly increased survival rate and improved the cardiac functions without changing the decreased Ca^<2+> sensitivity in DCM mouse. ARB also improved the fibrosis and electrocardiogram, which were considered as critical for the beneficial effects of ARB.
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