Investigation of the role of the fibrinolytic system in isehemic diseases
纤溶系统在缺血性疾病中作用的研究
基本信息
- 批准号:14570649
- 负责人:
- 金额:$ 2.24万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2002
- 资助国家:日本
- 起止时间:2002 至 2003
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We investigated the role of fibrinolyitc system in ischemic diseases. We obtained the results as follows:1.Lack of α2-antiplasmin decreases survival ratio after acute myocardial infarction. This phenomenon is due to mainly to the alteration of vascular permeability via an over-release of vascular endothelial growth factor (VEGF) as a result of the exaggerated activity of plasmin no longer tempered by α2 -antiplasmin.2.Lack of α2-antiplasmin improves the vascular patency after endothelial injury which is mainly because of the enhancement of endothelial cell healing via an over-release of VEGF.
我们研究了纤溶系统在缺血性疾病中的作用。我们得到的结果如下:1。α - 2抗纤溶酶缺乏降低急性心肌梗死后生存率。这种现象主要是由于α2 -抗纤溶酶无法调节的纤溶酶活性过高,导致血管内皮生长因子(VEGF)过度释放,从而改变了血管通透性。缺乏α2-抗纤溶酶可改善内皮细胞损伤后的血管通畅,这主要是通过过度释放VEGF促进内皮细胞愈合。
项目成果
期刊论文数量(44)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Takei M, Matsuno H, Okada K, Ueshima S, Matsuo O, Kozawa O: "Lack of α2-antiplasmin enhances ADP induced platelet micro-aggregation through the presence of excess active plasmin in mice."J.Thromb.Thrombolys. 14. 205-211 (2002)
Takei M、Matsuno H、Okada K、Ueshima S、Matsuo O、Kozawa O:“缺乏 α2-抗纤溶酶会通过小鼠体内过量的活性纤溶酶增强 ADP 诱导的血小板微聚集。”J.Thromb.Thrombolys 14。 205-211 (2002)
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Matsuno H, Kozawa O, Yoshimi N, Akamatsu S, Hara A, Mori H, Okada K, Matsuo O, Uematsu T: "Lack of α2-antiplasmin promotes pulmonary heart failure via over-release of VEGF after acute myocardial infarction"Blood. 100. 2487-2493 (2002)
Matsuno H、Kozawa O、Yoshimi N、Akamatsu S、Hara A、Mori H、Okada K、Matsuo O、Uematsu T:“急性心肌梗死后缺乏 α2-抗纤溶酶通过 VEGF 过度释放促进肺心力衰竭”血液。 100. 2487-2493 (2002)
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Matsuno H, Kozawa O, Okada K, Ueshima S, Matsuo O, Uematsu T.: "Inhibitors of fibrinolytic components play different roles in the formation and removal of arterial thrombus in mice."J.Cardiovasc.Pharmacol.. 39. 278-286 (2002)
Matsuno H、Kozawa O、Okada K、Ueshima S、Matsuo O、Uematsu T.:“纤溶成分的抑制剂在小鼠动脉血栓的形成和清除中发挥不同的作用。”J.Cardiovasc.Pharmacol.. 39. 278-
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- 发表时间:
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- 影响因子:0
- 作者:
- 通讯作者:
Takei M, Matsuno H, Okada K, Ueshima S, Matsuo O, Kozawa O.: "Lack of α2-antiplasmin enhances ADP induced platelet micro-aggregation through the presence of excess active plasmin in mice."J.Thromb.Thrombolysis. 14. 205-211 (2002)
Takei M、Matsuno H、Okada K、Ueshima S、Matsuo O、Kozawa O.:“缺乏 α2-抗纤溶酶会通过小鼠体内过量的活性纤溶酶增强 ADP 诱导的血小板微聚集。”J.Thromb.Thrombolysis 14。 .205-211 (2002)
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- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Matsuno H, Kozawa O, Okada K, Ueshima S, Matsuo O, Uematsu T: "Inhibitors of fibrinolytic components play different roles in the formation and removal of arterial thrombus in mice"J. Cardiovasc. Pharmacol.. 39. 278-286 (2002)
Matsuno H、Kozawa O、Okada K、Ueshima S、Matsuo O、Uematsu T:“纤溶成分的抑制剂在小鼠动脉血栓的形成和清除中发挥不同的作用”J。
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KOZAWA Osamu其他文献
KOZAWA Osamu的其他文献
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{{ truncateString('KOZAWA Osamu', 18)}}的其他基金
Molecular targets of low-molecular-weight heat shock proteins in hepatocellular carcinoma cell proliferation
低分子量热休克蛋白在肝癌细胞增殖中的分子靶点
- 批准号:
25460989 - 财政年份:2013
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Role of low-molecular-weight heat shock proteins and the molecular mechanism in hepatocellular carcinoma cell proliferation
低分子热休克蛋白在肝癌细胞增殖中的作用及分子机制
- 批准号:
22590726 - 财政年份:2010
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular mechanism of chaperone properties in bone metabolism
骨代谢伴侣特性的分子机制
- 批准号:
19591042 - 财政年份:2007
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Investigation of p20, a heat shock protein, in platelet function
研究 p20(一种热休克蛋白)在血小板功能中的作用
- 批准号:
11838005 - 财政年份:1999
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Investigation of stress response in osteoblasts
成骨细胞应激反应的研究
- 批准号:
09671041 - 财政年份:1997
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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