Fibrin is a nonwater-soluble, high-molecular-weight protein formed from fibrinogen (clotting factor I) during blood clotting by enzymatic action of thrombin. The medical specialties are histology and biochemistry.
What is fibrin?
During blood clotting, fibrin is formed from fibrinogen under the action of thrombin. Soluble fibrin, also called fibrin monomers, is formed, which polymerizes into a fibrin network by means of calcium ions and factor XIII. Fibrin molecules impede blood flow in a pathological process. Fibrinolysin dissolves the resulting blood clots. Fibrin is a protein and an important endogenous substance responsible for blood clotting. It is formed by the action of the clotting enzymes prothrombin and fibrinogen, which are produced in the liver. Fibrin consists of fiber-like molecules that are cross-linked together by a fine lattice. Fibrin lattices are an indispensable prerequisite of blood clotting. Medical terminology equally uses the terms plasma fibrin, blood fibrin, and globular plasma protein (serum proteins, blood proteins).
Anatomy and structure
No finished fibrin exists in blood, only the soluble precursor fibrinogen. Normally, the solid and liquid components of blood do not separate readily. When the blood leaves the body, long fibrin fibers are formed that spin the blood cells into a clot in the form of a blood cake. This process is indispensable for regularly functioning blood clotting. The escaping platelets stick to the fibrin fibers of the wound edges. After a bleeding time of about three minutes, sufficient platelets adhere to each other at the site of injury to form a blood clot that stops the bleeding. The network of fibrin threads that form gives the wound plug the necessary strength. Fibrin causes blood clotting through its ability to undergo cross-linking polymerization (reaction processes that lead to the formation of molecular substances). Thus, fibrin is one of the blood clotting factors. These substances are causative for blood clotting after injuries and ensure that bleeding is stopped. There are various blood clotting factors, designated by the numbers I to XIII. Fibrinogen is the most important clotting factor I. Blood clotting in the body proceeds in a cascade. To stop bleeding and cause blood clotting, fibrinogen is converted into fibrin. This forms chain-like structures that stabilize the blood clot. Fibrinogen forms the non-cross-linked precursor of fibrin. After an injury, two small peptides (fibrinopeptides) are split off from it during blood clotting under the action of the serine protease thrombin, converting it into monomeric fibrin. Subsequently, the polymeric fibrin is formed from this covalent cross-linking with the participation of calcium (calcium ions) and blood coagulation (factor XIII). As a result, a fibrin scaffold is formed to which platelets, erythrocytes and leukocytes adhere, leading to thrombus formation. Plasmin enables the subsequent degradation of the fibrin (fibrinolysis). Fibrinogen is one of the acute-phase proteins that can indicate inflammation in the body. The human body has thirteen clotting factors: Factor I fibrinogen, Factor II prothrombin, Factor III tissue thrombokinase, Factor IV calcium, Factor V proaccelerin, Factor VI corresponds to activated factor V, Factor VII proconvertin, Factor VIII hemophilia – A factor, lacks hemophilia, Factor IX hemophilia – B factor, Factor X Stuard power factor, Factor XI Rosenthal factor, Factor XII Hagemann factor, Factor XIII fibrin stabilizing factor. This classification is not identical with the order of activation in blood clotting. The reaction steps occur in different ways depending on the injury. The clotting factors are aligned so that, when activated, they undergo precisely coordinated steps in a chain reaction to produce fibrin.
Function and tasks
The coagulation system protects the body against bleeding to death by rapidly stopping bleeding from smaller vessels. The body’s own protein, plasma fiber, aids in this process and acts like a glue. A normally intact vascular system is not only at risk in the case of injuries caused by external influences that are immediately visible.The smallest vessels in the human body are regularly injured or leak, for example as a result of impacts or inflammation. The arterial vascular system is constantly under pressure. For this reason, even the smallest vascular injuries are likely to cause bleeding out of the vessel. To prevent this process, the coagulation system seals these leaking vessels from the inside. The clotting mechanism proceeds in several stages by controlling blood plasma substances in the form of clotting factors (I to XIII). Three reaction sequences form a chain reaction. The vascular reaction restricts blood loss by constricting the affected blood vessel. The platelet plug induces hemostasis by short-term vessel occlusion. Long-term vessel occlusion occurs through the formation of a fibrous network of fibrin. In the liver, the clotting proteins prothrombin as a precursor of thrombin and fibrinogen as a precursor of fibrin are formed. These two substances enter the blood plasma. The blood plasma is transformed into prothrombin with the help of the enzymes blood thrombokinase, tissue thrombokinase and calcium ions. This becomes thrombin and fibrinogen becomes fibrin. Fibrin forms the tissue mesh essential for hemostasis and stops bleeding.
Diseases
If the human coagulation system no longer works properly, severe disorders occur that severely restrict blood circulation. Depending on the underlying disorder, excessive blood thickening can lead to the formation of blood clots such as thrombosis and embolism. Excessive blood thickening causes an increased tendency to bleed or life-threatening bleeding. Causes may include both inherited and platelet or clotting factor disorders. Occasionally, clotting problems occur as a symptom of other conditions or diseases independent of the coagulation system, such as injury. Fibrinogen is determined in suspected cases of various diseases when the patient has an excessive tendency to bleed (hemorrhagic diathesis) or a tendency to form blood clots (thrombosis). Furthermore, fibrin is determined during treatment with streptokinase (extracellular protein, antigen) or urokinase (plasminogen activator, enzyme of the peptidases) to dissolve a blood clot (fibrinolysis therapy) for monitoring purposes and in the case of pathological activation of blood coagulation (consumption coagulopathy). The value is determined from blood plasma.
