Plasminogen activator inhibitor (PAI)-1 in vascular inflammation and thrombosis
Plasminogen activator inhibitor (PAI)-1 in vascular inflammation and thrombosis
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DOI：
10.2741/2285
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发表时间：
2007-05-01
影响因子：
3.1
通讯作者：
Aso, Yoshimasa
中科院分区：
文献类型：
--
作者：
Aso, Yoshimasa
纤维蛋白溶解受损可能与代谢综合征或2型糖尿病患者动脉粥样硬化血栓形成性心血管疾病（CVD）的发生有关。血浆纤溶酶原激活物抑制剂（派）-1是一种有效的纤溶抑制剂，在许多与CVD高发相关的临床情况下升高。高血浆派-1导致的纤维蛋白溶解受损可导致血管内纤维蛋白过度积聚，导致动脉粥样硬化血栓形成。派-1的表达增加见于人类动脉粥样硬化病变，尤其是2型糖尿病患者的动脉粥样硬化斑块。派-1在血管中表达的增加通过抑制血小板-纤维蛋白血栓的清除而导致纤维蛋白或纤维蛋白原的积累，从而促进新生内膜的形成。急性时相蛋白派-1也可能参与血管炎症反应。派-1可能不仅与全身相关，而且与CVD的发展局部相关。
Impaired fibrinolysis may be associated with development of atherothrombotic cardiovascular disease ( CVD) in metabolic syndrome or type 2 diabetes. Plasma plasminogen activator inhibitor (PAI)-1, a potent inhibitor of fibrinolysis, is elevated in a number of clinical situations that are associated with high incidence of CVD. Impaired fibrinolysis resulting from high plasma PAI-1 can lead to excessive fibrin accumulation within vessels, resulting in atherothrombosis. Increased expression of PAI-1 is found in atherosclerotic lesions in humans, especially atherosclerotic plaques in patients with type 2 diabetes. This increased vascular expression of PAI-1 promotes neointima formation via accumulation of fibrin or fibrinogen as a result of inhibited clearance of platelet-fibrin thrombi. PAI-1, an acute phase protein, also could be involved in vascular inflammation. PAI-1 may be associated not only systemically but also locally with development of CVD.