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Fibrinogen is made and secreted into the blood primarily by liver hepatocyte cells. Endothelium cells are also reported to make small amounts of fibrinogen, but this fibrinogen has not been fully characterized; blood platelets and their precursors, bone marrow megakaryocytes, while once thought to make fibrinogen, are now known to take up and store but not make the glycoprotein.
Fibrillogenesis is the development of fine fibrils normally present in collagen fibers of connective tissue.It is derived from the New Latin fibrilla (meaning fibrils, or pertaining to fibrils) and Greek genesis (to create, the process by which something is created).
Fibrosis, also known as fibrotic scarring, is a pathological wound healing in which connective tissue replaces normal parenchymal tissue to the extent that it goes unchecked, leading to considerable tissue remodelling and the formation of permanent scar tissue.
Fibrin monomers are monomers of fibrin which are formed by the cleavage of fibrinogen by thrombin. [1] Levels of fibrin monomers can be measured using blood tests and can serve as a marker of in vivo fibrinogenesis and coagulation activation.
Coagulation activation markers are biomarkers of net activation of coagulation and fibrinolysis. [1] [2] Examples include prothrombin fragment 1+2 (F1+2), thrombin–antithrombin complex (TAT), fibrinopeptide A (FpA), fibrin monomers (FMs), plasmin-α 2-antiplasmin complex (PAP), activated protein C–protein C inhibitor (APC-PCI), and D-dimer (DD).
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Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot.It results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair.
The fibrinopeptides, fibrinopeptide A (FpA) and fibrinopeptide B (FpB), are peptides which are located in the central region of the fibrous glycoprotein fibrinogen (factor I) and are cleaved by the enzyme thrombin (factor IIa) to convert fibrinogen into covalently-linked fibrin (factor IA) monomers.