Cardiovascular disease, Extracellular matrix, Renal disease
Fibrinogen alpha (FGA), fibrinogen beta (FGB), and fibrinogen gamma (FGG) polymerize to form an insoluble fibrin matrix. Fibrin has a major function in hemostasis as one of the primary components of blood clots. In addition, fibrin functions during the early stages of wound repair to stabilize the lesion and guide cell migration during re-epithelialization. Fibrin was originally thought to be essential for platelet aggregation, based on in vitro studies using anticoagulated blood. However, subsequent studies have shown that it is not absolutely required for thrombus formation in vivo. Fibrin enhances expression of SELP in activated platelets via an ITGB3-dependent pathway. Maternal fibrinogen is essential for successful pregnancy. Fibrin deposition is also associated with infection, where it protects against IFNG-mediated hemorrhage. Fibrin may also facilitate the immune response via both innate and T-cell mediated pathways.
Fibrinolysis is the enzymatic breakdown of fibrin in blood clots. Plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases. Primary fibrinolysis is a normal body process. The fibrinolytic system serves to limit the formation of thrombi and to facilitate healing or recanalization of a vessel with a thrombotic occlusion. Secondary fibrinolysis is the breakdown of clots due to medicine, disorder, or other cause.
Under normal conditions, the fibrinolytic process is localized on the fibrin clots because alpha2-antiplasmin and the plasminogen activator inhibitors prevent fibrinolysis from spreading. Fibrin Degradation Products (FDP) that occur are very heterogeneous and include products derived from fibrin, soluble complexes, degradation products from fibrinogen, and from nonstabilized fibrin. The presence FDP of in plasma can provide important information for the diagnosis of hemostatic disorders. An abnormal fibrinolytic and/or fibrinogenolytic activity shown by high levels of FDP in plasma can be found in clinical states, such as eclampsia, carcinoma (promyelocytic leukemia), cardiac and renal disorders, hepatic disorders, fibrinolysis, pulmonary embolism, deep vein thrombosis (DVT), following surgery or trauma, and after lytic therapy.
Increased FDPs are seen in primary fibrinolysis as well as during fibrin clot breakdown. Elevated FDP levels are a hallmark finding in disseminated intravascular coagulation (DIC). Elevated FDP levels are not specific for DIC and increased FDP levels are often seen in primary fibrinolysis, severe liver disease, including alcoholic cirrhosis, eclampsia, during acute thrombotic episodes.