课题基金 / 基金详情

動脈硬化の分子機構

動脈硬化の分子機構
动脉硬化的分子机制
批准号:
09281104
负责人:
KITA Toru
金额:
$165.89万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research on Priority Areas (A)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 2001

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中文摘要
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英文摘要
The Grants-in-Aid for Scientific Research on Priority Areas No. 09281104 was issued from 1997 to 2000. During the period, we organized a research group with scientists who are considered to be most active in the research field. Atherosclerosis is correlated with a variety of vascular disorders such as coronary heart disease. We therefore placed our goal on elucidation of the molecular mechanism of atherosclerosis and exploration of novel therapeutic strategies. To conduct investigation, the members were divided into 3 subgroups, i.e. Group 1, 2, and 3 with different subject of study as follows. We also formed a Central Committee to coordinate and facilitate the research activity of the subgroups.[Group 1] Study subject : Molecular mechanism of vascular formation. Atherosclerosis has been considered to evolve according to the mechanism shared with vascular formation in the body. During the research period, we have made a significant progress in understanding vasculogenesis and angiogene … More sis. In Conclusion, the roles of new molecules such as transcription factor ets-1 and other molecules were clarified. [Group 2] Study subject : Endothelial dysfunction and blood cells. There has been accumulating evidence that atherosclerosis is initiated by endothelial dysfunction due to a variety of biological insults. We therefore formed this subgroup to explore the key molecules involved in those events. We discovered novel scavenger receptors such as LOX-1 and SRPSOX. Furthermore, we revealed that adipose tissues produce cytokines abundantly. Among those cytokines, adiponectin has been shown to play an important role in atherogenesis and insulin resistance. [Group 3] Study subject : Molecular mechanism of phenotypical conversion and proliferation of vascular smooth muscle cells. This subgroup focused on the mechanism of phenotypical conversion of vascular smooth muscle cells, which is believed to be the characteristic feature of the advanced atherosclerotic lesions. To clarify these points, a variety of transcription factors such as BTBE2 were examined. Also, the new methods to deliver genes were developed.In conclusion, we have made a successful progress in atherosclerosis research, which will be translated into clinical application in the near future. Less
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Minami, M., Kume, N., et al.: "Expression of SR-PSOX, a novel cell-surface receptor for atherogenic oxidized low density lipoprotein, in human atherosclerotic lesions"Arterioscler.Thromb.Vasc.Biol.. 21. 1796-1800 (2001)
Minami, M., Kume, N. 等人:“SR-PSOX 的表达,一种新型细胞表面致动脉粥样硬化氧化低密度脂蛋白受体,在人动脉粥样硬化病变中的表达”Arterioscler.Thromb.Vasc.Biol.. 21。
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Kanaki, T., Bujo, H. et al.: "Expression of LR11, a mosaic LDL receptor family member, is markedly increased in atherosclerotic lesions"Arterioscler. Thromb. Vasc. Biol.. 19. 2687-2695 (1999)
Kanaki, T., Bujo, H. 等人:“LR11(一种嵌合 LDL 受体家族成员)的表达在动脉粥样硬化病变中显着增加”Arterioscler。
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Wakiya,K.et al.: "A cyclic AMP response element and an ETS motif are involved in the transcreptional regulation 0 flt-1 tyrosine kinase (VEGF receptor 1) gene." J.Biol.Chem.271. 30823-30828 (1996)
Wakiya,K. 等人:“环状 AMP 反应元件和 ETS 基序参与转录调节 0 flt-1 酪氨酸激酶(VEGF 受体 1)基因。”
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Sano, H., Sudo, T., Yokode, M., et al.: "Functional Blockade of Platelet-derived Growth Factor Receptor-β but Not of Receptor-α Prevents Vascular Smooth Muscle Cell Accumulation in the Fibrous Cap Lesions in Apolipoprotein E-deficient Mice"Circulation. 10
Sano, H.、Sudo, T.、Yokode, M. 等人:“功能性阻断血小板衍生生长因子受体-β 但不阻断受体-α 可防止载脂蛋白纤维帽病变中血管平滑肌细胞积聚E-缺陷小鼠”循环。10
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35
    Molecular mechanism of the process from atherosclerotic lesion formation to plaque rupture
    • 批准号:
      16209031
    • 项目类别:
      Grant-in-Aid for Scientific Research (A)
    • 资助金额:
      $32.28万
    • 财政年份:
      2004
    • 负责人:
      KITA Toru
    • 依托单位:
    Cell biological study for atherosclerosis
    • 批准号:
      11694266
    • 项目类别:
      Grant-in-Aid for Scientific Research (A).
    • 资助金额:
      $4.99万
    • 财政年份:
      1999
    • 负责人:
      KITA Toru
    • 依托单位:
    Molecular mechanism of activation of endothelial cells involved in early stage of atherosclerosis formation.
    • 批准号:
      11307018
    • 项目类别:
      Grant-in-Aid for Scientific Research (A).
    • 资助金额:
      $23.55万
    • 财政年份:
      1999
    • 负责人:
      KITA Toru
    • 依托单位:
    Molecular Mechanism of Atherosclerosis
    • 批准号:
      09281103
    • 项目类别:
      Grant-in-Aid for Scientific Research on Priority Areas (A)
    • 资助金额:
      $128.06万
    • 财政年份:
      1997
    • 负责人:
      KITA Toru
    • 依托单位:
    海外基金