| Project/Area Number |
16K09508
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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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| Research Field |
Cardiovascular medicine
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
Sakamoto Masaya 東京慈恵会医科大学, 医学部, 准教授 (40419742)
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| Co-Investigator(Kenkyū-buntansha) |
武田 憲彦 東京大学, 医学部附属病院, 助教 (40422307)
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| Research Collaborator |
Matsutani Diasuke
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 圧受容器機能 / 糖尿病 / 圧受容器 / 血圧変動 / 12-LOX / 2型糖尿病 / 心不全 / 高血圧 / 循環器・高血圧 |
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| Outline of Final Research Achievements |
In type 2 diabetes, the molecular mechanism by which an increase in blood pressure fluctuation due to dysfunction of baroreceptor function causes myocardial remodeling is unknown. We developed a unique in vivo model (Sino-aortic denervation (SAD)) in which type 2 diabetes model rat (GK / Slc) was combined with increased blood pressure fluctuation, and newly developed rat primary rat cultured cells and fibroblasts. The analysis was performed using the in vitro blood pressure fluctuation stimulator. As a result, it was found that 12-LOX, which is one pathway of the arachidonic acid cascade, is involved in the mechanism, and suppression of its expression results in improvement of myocardial fibrosis and function.
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| Academic Significance and Societal Importance of the Research Achievements |
糖尿病合併心不全の予後は以前として悪化の一途を辿っている。今回12ーlipoxygenaseがその発生に関与している事が明らかとなった。既存の薬剤にておいても一部その発現に関与していることも明らかとなった。ヒトにおいても圧受容器の機能測定が可能となっており、今後の臨床応用により糖尿病患者の予後改善へと結びつける研究の一助となった。
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