| Project/Area Number |
21590893
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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 |
Circulatory organs internal medicine
|
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| Research Institution | Osaka University |
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Principal Investigator |
SAKATA Yasushi 大阪大学, 医学系・研究科, 講師 (00397671)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Kazuhiro 鳥取大学, 医学部, 教授 (90303966)
MANO Toshiaki 大阪大学, 医学部附属病院, 講師 (90379165)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 心不全 / 拡張機能 / 食塩感受性 / 内因性ステロイド |
|---|
| Research Abstract |
The production of CTS was enhanced in hypertensive HFPEF model. Ouabain activated p42/ 44 MAPKs and enhanced collagen production through the elevation of cytosolic Ca^<2+> concentration via NCX entry mode. SEA0400, the potent inhibitor of NCX entry mode, prevented the development of LV fibrosis and stiffening and the transition to HFPEF with the improvement of survival rate in the animal models. Thus, CTS and the subsequently activated Ca^<2+> entry mode of NCX may play an important role in the development of LV fibrosis and hypertensive HFPEF, and the blockade of the entry mode of NCX is likely a new therapeutic strategy for this phenotype of heart failure.
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