Lijnen H R, Collen D
Center for Molecular and Vascular Biology, K.U. Leuven, Belgium.
Prog Cardiovasc Dis. 1997 Jan-Feb;39(4):343-50. doi: 10.1016/s0033-0620(97)80032-1.
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.
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。
