因子 VIIa 与内皮细胞及内皮细胞蛋白 C 受体的相互作用。
Factor VIIa interaction with endothelial cells and endothelial cell protein C receptor.
机构信息
Center for Biomedical Research, The University of Texas Health Science Center at Tyler, TX 75708, USA.
出版信息
Thromb Res. 2010 Apr;125 Suppl 1:S19-22. doi: 10.1016/j.thromres.2010.01.026. Epub 2010 Feb 14.
Abstract
Plasma coagulation factor VIIa (FVIIa) initiates the coagulation cascade by binding to its cofactor, tissue factor (TF) on cell surfaces, which eventually leads to fibrin deposition and platelet activation. Recent studies showed that FVIIa also binds to endothelial cell protein C receptor (EPCR), a known cellular receptor for anticoagulant protein C\activated protein C, on the endothelium. The present article reviews our current knowledge of FVIIa interaction with EPCR and discusses the potential significance of this interaction in hemostasis, treatment of bleeding disorders with pharmacological doses of FVIIa and FVIIa clearance.
摘要
血浆凝血因子 VIIa (FVIIa) 通过与细胞表面的辅助因子组织因子 (TF) 结合启动凝血级联反应，最终导致纤维蛋白沉积和血小板激活。最近的研究表明，FVIIa 还与内皮细胞蛋白 C 受体 (EPCR) 结合，EPCR 是已知的抗凝蛋白 C\激活蛋白 C 的细胞受体。本文综述了我们目前对 FVIIa 与 EPCR 相互作用的认识，并讨论了这种相互作用在止血、用药理学剂量的 FVIIa 治疗出血性疾病和 FVIIa 清除方面的潜在意义。
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