| Project/Area Number |
25860586
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 自然炎症 / 心肥大 / 心不全 / TLR2 / 熱ショック蛋白質 / IL-1β / NLRP3 / インフラマソーム / 適応応答 / 炎症 / NF-κB / IL-１β |
|---|
| Outline of Final Research Achievements |
To investigate the role of homeostatic inflammation in cardiac hypertrophy, we assessed the role of pattern recognition receptors in the pathophysiology of pressure overload-induced cardiac hypertrophy. We clarified that Toll-like receptor 2-mediated interleukin 1β production, induced by extracellularly released heat shock protein 70, is essential for adaptive cardiac hypertrophy in response to pressure overload. In addition, we found that the NLRP3 inflammasome, a multiprotein complex involved in the innate immune response, regulates active IL-1β production in the heart during pressure overload and contribute to adaptive cardiac hypertrophy. These results revealed the essential role and the underlying mechanisms of homeostatic inflammation in the pathophysiology of pressure overload-induced cardiac hypertrophy.
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