| Project/Area Number |
18K08048
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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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| Review Section |
Basic Section 53020:Cardiology-related
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| Research Institution | Keio University |
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Principal Investigator |
ANZAI Atsushi 慶應義塾大学, 医学部(信濃町), 助教 (50528164)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 心筋梗塞 / 炎症 / 免疫応答 / 心外膜脂肪 / 免疫 / 心不全 |
|---|
| Outline of Final Research Achievements |
We identified that interleukin (IL)-3-expressing B cells expand in the pericardial fat in response to myocardial infarction in mice. IL-3 receptor is highly expressed in cardiac macrophages and inflammatory monocytes. In vitro experiments using bone marrow-derived macrophages further revealed that IL-3 stimulates them to produce inflammatory cytokines and chemokines such as IL-1beta, IL-6, and CCL2, suggesting that pericardial B cell-derived IL-3 accelerates infarct inflammation, thereby leading to poor outcomes.
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| Academic Significance and Societal Importance of the Research Achievements |
循環器疾患における心外膜脂肪の意義を示した研究は少ない。本研究はIL-3を介した心外膜脂肪と心臓monocytes/macrophageのクロストークが梗塞後の過剰な炎症を誘導・増幅する機序を示すのみならず、心外膜脂肪がどのように循環器疾患に影響を与えるのかを明らかにする研究になり得る。さらにはヒト検体を用いた臨床研究へ発展する可能性を秘めており、心筋梗塞後心不全を予防する新規治療法開発に繋がる可能性がある。
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