| Project/Area Number |
18K11036
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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 59040:Nutrition science and health science-related
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| Research Institution | Hiroshima International University |
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Principal Investigator |
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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 |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | AGEs / 血管内皮細胞 / グリセルアルデヒド / 血管透過性 / RasGRP2 / AGEｓ / 終末糖化産物 / ＡＧＥｓ |
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| Outline of Final Research Achievements |
Vascular disorder is a major event common to diabetic complications, and one of the causes is advanced glycation end products (AGEs). However, the therapeutic agents and AGEs formation inhibitors have not yet been developed and hasn't reached a basic resolution. So far, we have found that RAS guanyl nucleotide-releasing protein 2 (RasGRP2), a guanine nucleotide exchange factor, which activates small GTPases, is expressed in vascular endothelial cells and suppresses apoptosis via the Rap1 and R-Ras pathways. Furthermore, in this study, we clarified that RasGRP2 may act as a protective factor for vascular disorder by suppressing the vascular hyper-permeability caused by AGEs via both pathways.
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| Academic Significance and Societal Importance of the Research Achievements |
現代の食生活や社会環境下において糖尿病を根絶することはほぼ不可能に近く、疾患そのものの克服だけでなく重症化予防についても目を向けて行かなければならない。今回の研究成果は、AGEsによる血管障害における防御メカニズムとして新たな知見を見出しており、糖尿病合併症による重症化を防ぐ画期的な予防薬の開発に繋がると期待される。
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