Tissue Factor, Blood Coagulation, and Beyond: An Overview

Figure 2

TF hypercoagulability and inflammation. TF-initiated extrinsic coagulation (left panel) essentially proceeds as extracellular signaling and results in the generation of active serine protease (coagulant mediators: FVIIa, FXa, and FIIa) derived from their corresponding zymogen activations. FBG is cleaved by FIIa to produce fibrin that is polymerized and cross-linked to yield insoluble blood clots. Such TF extracellular signaling activates cells for proinflammation. Through cell receptors on plasma membrane, signals from the coagulant mediators (FVIIa, FXa, and FIIa) as well as fibrin mediate diverse intracellular activation and the production of proinflammatory mediators (right panel) including cytokines, adhesion molecules, and growth factors, PAR: protease activated receptor; TLR: Toll-like receptor; IL: interleukin; NFκB: nuclear factor kappa B.