| Project/Area Number |
17K16030
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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 | Kurume University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 慢性肺血栓症 / 慢性肺血栓塞栓症 / 内皮障害 / 線溶系異常 / 肺循環 / 慢性血栓塞栓性肺高血圧症 / 慢性血栓塞栓性肺高血圧 / 血管内皮障害 / 循環器内科学 |
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| Outline of Final Research Achievements |
The purpose of this study is to investigate whether both fibrinolytic and endothelial dysfunction are related to the onset of chronic pulmonary thromboembolism. Although we tried to create a model mouse for chronic pulmonary thromboembolism, it was poorly reproducible. However, pulmonary hypertension remained in the process of creating this model. Therefore, we are focusing on the biological reaction of pulmonary artery endothelial cells to thrombus, and we will elucidate the mechanism of the ability of vascular endothelial cells to phagocytose foreign substances in blood vessels and excrete them out of blood vessels.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の学術的意義は組織プラスミノーゲンアクチベーター(tPA)に関連した線溶系異常と一酸化窒素合成酵素(NOS)障害に関連した内皮障害の双方を有していても、慢性肺血栓塞栓症のモデルマウスを作成することが困難であったことを示したことである。また、異物に対する内皮機能であるAngiophagyの研究を肺血管内皮細胞で試みたことにも学術的意義がある。慢性肺血栓塞栓症のモデルマウスの作成やAngiophagyと慢性肺血栓塞栓症の関連を示すまでに現時点で至らなかったことから、本研究の社会的意義の判断は難しい。
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