Investigation of the role of physiological hypertrophy in the transition from compensatory hypertrophy to heart failure
| Project/Area Number |
16H07049
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
IKEDA MASATAKA 九州大学, 医学研究院, 学術研究員 (10567382)
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 心不全 / 低酸素 / REDD1 / DDIT4 / 慢性心不全 / 生理的心肥大 / mTOR / 低酸素誘導因子 / 心肥大 / 心臓リモデリング |
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| Outline of Final Research Achievements |
In this study, we investigated the role of REDD1 in the transition from compensatory hypertrophy to heart failure (HF), by focusing on intracellular changes, particularly Hif-1α and REDD1, in response to hypoxia induced by excessive hypertrophy.
Hif-1α and REDD1 were upregulated in the failing myocardium of HF models. In isolated cardiomyocytes, 1% hypoxia induced cell death, accompanied by increased Hif-1α and REDD1, while the knockdown of REDD1 using siRNA aggravated it. Taken together, these results suggested that REDD1, which increased in response to hypoxia induced by excessive hypertrophy in HF, plays a protective role in the failing myocardium.
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Report
(3 results)
Research Products
(4 results)
