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止血与血栓形成中的内皮

Endothelium in hemostasis and thrombosis.

作者信息

Lijnen H R, Collen D

机构信息

Center for Molecular and Vascular Biology, K.U. Leuven, Belgium.

出版信息

Prog Cardiovasc Dis. 1997 Jan-Feb;39(4):343-50. doi: 10.1016/s0033-0620(97)80032-1.

Abstract

Endothelial cells synthesize and secrete PA and PAI, and thus provide anticoagulant and procoagulant regulatory mechanisms, respectively. Both plasminogen and plasminogen activators (t-PA and u-PA) bind to specific cellular receptors; assembly of components of the fibrinolytic system at the endothelial cell surface results in stimulation of fibrinolytic activity. Several mechanisms contribute to this stimulation, eg, enhanced plasminogen activation by t-PA or u-PA, enhanced conversion of scu-PA to tcu-PA, and impaired inhibition of plasmin by alpha2-antiplasmin or of PAs by PAIs. Thus, the endothelial cell surface serves as a focal point for plasmin generation.

摘要

内皮细胞合成并分泌纤溶酶原激活物(PA)和纤溶酶原激活物抑制剂(PAI),从而分别提供抗凝和促凝调节机制。纤溶酶原和纤溶酶原激活物(组织型纤溶酶原激活物(t-PA)和尿激酶型纤溶酶原激活物(u-PA))均与特定的细胞受体结合;纤溶系统的成分在内皮细胞表面组装会导致纤溶活性增强。有几种机制促成了这种增强,例如,t-PA或u-PA介导的纤溶酶原激活增强、单链尿激酶型纤溶酶原激活物(scu-PA)向双链尿激酶型纤溶酶原激活物(tcu-PA)的转化增强,以及α2-抗纤溶酶对纤溶酶或PAI对PA的抑制受损。因此,内皮细胞表面是纤溶酶生成的焦点。

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