| Project/Area Number |
26670177
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Human pathology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鬼丸 満穂 九州大学, 医学研究院, 助教 (00380626)
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| Co-Investigator(Renkei-kenkyūsha) |
SUEISHI KATSUO 国立病院機構福岡東医療センター, 研究教育部長 (70108710)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 病理学 / 循環器 / 動脈硬化 / Ｄアスパラギン酸 / 石灰化 / 血管リモデリング / 終末糖化産物 / 血管平滑筋細胞 |
|---|
| Outline of Final Research Achievements |
Early stages of atherosclerosis develop not by SMC migration and proliferation, but by dispersion of intimal SMCs, that were caused by the macrophage infiltration and the lipid pool formation without undergoing significant proliferation or death. Formation of non-enzymatic chemical products (D-aspartic acid or Advanced glycation end products(AGEs)) in intima would associate with matrix degradation or calcification. As results, accumulation of these errors in vascular wall pull the trigger of pathogenesis, and affects the advanced fate of atherosclerosis.
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