| Project/Area Number |
15K10618
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 越 聖マリアンナ医科大学, 医学研究科, 講師 (40313134)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 動脈硬化 / プラーク内出血 / 炎症性サイトカイン / エピジェネティックス / IL-1beta siRNA / ApoE欠損マウス / マイクロRNA / 器質性勃起障害 |
|---|
| Outline of Final Research Achievements |
The rupture of plaques in atherosclerotic lesion causes the obstruction of the coronary artery, leading to acute myocardial infarction. Therefore, it is pivotal to establish a method to prevent plaque rupture. It is well known that plaques with thin-cap fibroatheroma is vulnerable to damages and often rupture. Intraplaque hemorrhage (IPH) is regarded as a major factor that triggers the instability and vulnerability of plaques. We found that the proinflammatory cytokine interleukin-1beta（IL-1beta）is implicated in IPH using a mouse model of atherosclerosis. We also found that IL-1beta inhibits normal angiogenesis and stimulates immature angiogenesis, which results in the leakage of erythrocytes from new vessels in the plaques and IPH.
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| Academic Significance and Societal Importance of the Research Achievements |
急性心筋梗塞は代表的な心血管病であり発症を防ぐことは国民の健康寿命を延ばすために重要である。今回我々はマウスのモデルではあるが炎症性サイトカインであるinterleukin-1beta（IL-1beta）の発現を抑制すると急性心筋梗塞の発症を予防できる可能性を示すことができた。今後IL-1betaの阻害薬あるいは活性阻害抗体薬などが開発されることを期待したい。
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