课题基金 / 基金详情

DEFINING STRATEGIES FOR IMPROVING ENDOTHELIAL/FIBRINOLYTIC DYFUNCTION IN OBESITY

DEFINING STRATEGIES FOR IMPROVING ENDOTHELIAL/FIBRINOLYTIC DYFUNCTION IN OBESITY
制定改善肥胖症内皮/纤溶功能障碍的策略
批准号:
7731488
负责人:
Douglas E Vaughan
金额:
$0.05万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-12-01 至 2007-09-16

项目摘要

项目成果

Douglas E Vaughan的其他基金

相关文献

中文摘要
翻译
这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金, 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 中心假说是血管内PAI-1过量促进血管内血栓的形成。我们将测试脂肪细胞分泌的因子是否具有自分泌、旁分泌和内分泌作用,对纤溶系统产生有害影响,无论是通过促进PAI-1的产生,还是通过损害内皮t-PA的释放。
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The central hypothesis is that vacular PAI-1 excess promotes the development of intravascular thrombosis. We will test that secreted factors from adiocytes have autocrine, paracrine, and endocrine effects that have deleterious effect on the fibrinolytic system, either by enhancing PAI-1 production or impairing endothelial t-PA release.
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会议论文
Evolutionary Advantage of Heterozygous PAI-1 Deficiency in Humans
Spontaneous cardiac fibrosis in PAI-1-deficient mice and men: A rare mutation informs a common molecular pathophysiology
Spontaneous cardiac fibrosis in PAI-1-deficient mice and men: A rare mutation informs a common molecular pathophysiology
Cardiovascular Regenerative Medicine