2022 Fiscal Year Final Research Report
High risk coronary plaque for acute myocardial infarction: who is a culprit of increased thrombogenicity
| Project/Area Number |
19K16560
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 49020:Human pathology-related
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2023-03-31
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| Keywords | 動脈硬化 / 血栓症 / マクロファージ / 低酸素 / 心筋梗塞 |
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| Outline of Final Research Achievements |
The purpose of this study is (1) the involvement of hypoxia in the expression of tissue factor in coronary artery plaques, and (2) the molecular biological mechanisms by which hypoxia promotes thrombus formation.
(1) In a study using coronary artery specimens from autopsy cases, macrophages were more abundant in “vulnerable plaques” than in “stable plaques,” and the expression and localization of tissue factor and hexokinase 2 in plaques were associated with macrophages. (2) In cultured macrophages, hypoxia increased the coagulation activity of cells induced by inflammatory stimulation. The effect was also abolished by inhibition of glycolysis.
Based on the above, hypoxia-induced glycolytic metabolism was considered to contribute to plaque thrombus formation.
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| Free Research Field |
人体病理学
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| Academic Significance and Societal Importance of the Research Achievements |
急性心筋梗塞の原因となる動脈硬化は喫煙、ストレス、高血圧、脂質異常や糖尿病により進展することがしられている。さらにプラークの血栓形成能を増大させる機序が明らかとなれば、予防的介入の選択肢が広がり、国民の健康に貢献できる可能性が期待される。
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