Fibrinogen–thrombin coagulation pathway

The fibrinogen–thrombin coagulation pathway is the terminal sequence of the blood coagulation cascade, essential for the formation of stable blood clots [6, 11]. In this pathway, the serine protease thrombin (Factor IIa) catalyzes the conversion of soluble plasma fibrinogen (Factor I) into insoluble fibrin monomers [1, 16]. These monomers polymerize to form a fibrin mesh that stabilizes the primary platelet plug at the site of vascular injury [1, 11]. This process is a critical component of secondary hemostasis and is vital for wound healing and preventing hemorrhage [6, 16]. Pathological activation of this pathway is a major driver of thrombotic diseases, including deep vein thrombosis, pulmonary embolism, and myocardial infarction [1, 9]. Pharmacological intervention often targets this pathway using anticoagulants such as direct thrombin inhibitors (e.g., dabigatran) or indirect inhibitors like heparin [4, 10]. Additionally, thrombin within this pathway acts as a signaling molecule by activating protease-activated receptors (PARs) on platelets and endothelial cells [7, 14]. Fibrin also serves as a provisional matrix for cell migration and tissue repair during the inflammatory response [9, 12]. Monitoring the pathway's activity is clinically achieved through biomarkers such as D-dimer and fibrinogen levels [5, 7]. Overall, the fibrinogen–thrombin pathway is a central regulator of vascular integrity and a key therapeutic focus in cardiovascular medicine [1, 11].

Other names

Final common pathway of coagulationThrombin-fibrinogen interactionCoagulation cascade (final step)Thrombin-fibrinogen axis

Direct thrombin inhibition, indirect thrombin inhibition via antithrombin, inhibition of vitamin K-dependent factor synthesis, fibrinolysis, and fibrinogen replacement.