Duke University Durham Veterans Affairs Medical Centers Durham, NC, USA.
Division of Hematology/Oncology Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC.
Thromb Res. 2014 May;133 Suppl 1:S1-2. doi: 10.1016/j.thromres.2014.03.001.
Initiation of clotting cascade by tissue factor (TF): Factor VII (FVII) complex is essential for hemostasis however pathologic expression of TF leads to thrombosis. In contrast, the contact pathway factor XII, and to the smaller extent FXI are dispensable for normal hemostasis but still contribute to pathologic thrombosis. New data suggest that not only platelets but also leukocytes and red blood cells can actively participate to thrombosis. Growing evidence demonstrates that coagulation proteases not only regulate hemostasis and thrombosis but also contribute to the many cellular responses via activation of protease activated receptors (PARs). The reviews in this supplement summarize the latest findings related to TF and coagulation proteases, including novel models of hemostasis and thrombosis, new insights into mechanism of thrombosis and trauma induced coagulopathy, interplay between coagulation and innate immune system and pathophysiology of contact activation pathway.
组织因子(TF)引发凝血级联反应:VII 因子(FVII)复合物对于止血至关重要,但 TF 的病理表达会导致血栓形成。相比之下,接触途径因子 XII,以及较小程度的 FXI,对于正常止血是可有可无的,但仍有助于病理血栓形成。新数据表明,不仅血小板,而且白细胞和红细胞也可以积极参与血栓形成。越来越多的证据表明,凝血蛋白酶不仅调节止血和血栓形成,而且还通过激活蛋白酶激活受体(PARs)来促进许多细胞反应。本增刊中的综述总结了与 TF 和凝血蛋白酶相关的最新发现,包括止血和血栓形成的新模型、血栓形成和创伤诱导的凝血障碍机制的新见解、凝血与先天免疫系统的相互作用以及接触激活途径的病理生理学。