New Ca^<2+> entry pathway in the development of cardiac hypertrophy
| Project/Area Number |
22790199
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Akita University |
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Principal Investigator |
OHBA Takayoshi 秋田大学, 大学院・医学系研究科, 助教 (80431625)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | 受容体 / 細胞内シグナル伝達 / 心肥大 / カルシウム |
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| Research Abstract |
The purpose of this research is clarifying the new molecular mechanism of cardiac hypertrophy. I analyzed the phenotype and the mechanism of cardiac hypertrophy for STIM1 knockout mouse. The cardiac hypertrophy induced by transverse aortic constriction (TAC) was significantly inhibited in the STIM1+/. mice. Moreover, STIM1+/. TAC exhibited significant decrease in fibrosis and significant increase in survival rate compared with wild-type TAC. In conclusion, these results provide definitive evidence that STIM1 is crucial for cardiac hypertrophy and fibrosis induced by pressure overload in adult mice in vivo. This STIM1 signaling is an interesting target for treatment of cardiac hypertrophy and heart failure.
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Report
(4 results)
Research Products
(25 results)
