Elucidation of a switching mechanism between production and extinction of reactive oxygen species on vascular remodeling after injury
| Project/Area Number |
18K08115
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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 | Showa University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 動脈硬化 / 血管内膜肥厚 / 酸化ストレス / 血管平滑筋細胞 / Nrf2 / 骨髄細胞 / IQGAP1 / 活性酸素 |
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| Outline of Final Research Achievements |
Oxidative stress induces arteriosclerosis. Therefore, to elucidate regulatory mechanisms of reactive oxygen species production and elimination leads to prevention and treatment of ischemic diseases. In this study, IQGAP1, a receptor tyrosine kinase binding scaffolding protein, enhanced PDGF-induced vascular smooth muscle cell migration and neointimal thickening after vascular injury. Conversely, Nrf2, a key regulator of antioxidative enzymes, inhibited their events. These findings provide insight into IQGAP1 and Nrf2 as novel therapeutic targets for vascular remodeling and atherosclerosis.
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| Academic Significance and Societal Importance of the Research Achievements |
動脈硬化は、心筋梗塞や脳梗塞など、生命予後に直結する重大な病気の引き金となる。したがって、生体における酸化ストレスを制御メカニズムを解明することは、新たな動脈硬化の治療法につながる。本研究では、活性酸素産生を促進するIQGAP1および抗酸化酵素の発現に関わるNrf2の血管における機能解析を行ったところ、血管において、IQGAP1が動脈硬化の促進およびNrf2が抑制に関与することを明らかにした。これらの結果は、動脈硬化の治療標的となる可能性を示唆している。
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Report
(4 results)
Research Products
(18 results)
