Coagulation

Blood coagulation (haemostasis) is a physiological process that prevents excessive bleeding when blood vessels are injured, whilst simultaneously ensuring that the clotting process is controlled to prevent the formation of potentially dangerous blood clots. It involves a sequence of coordinated molecular and cellular events, mediated by a series of proteins known as clotting factors. When a blood vessel is injured, its associated smooth muscle cells first contract to reduce blood flow, which is an immediate response to limit blood loss. Platelets, small cell fragments, then adhere to the exposed subendothelial matrix of the injured vessel. This is controlled by a process involving von Willebrand factor (vWF) and platelet receptors, such as the glycoprotein Ib/IX/V complex. Upon adhesion, platelets become activated, change shape, and release granules containing factors that promote further platelet aggregation and clot formation. The coagulation cascade itself involves a series of sequential steps that lead to the conversion of inactive clotting factors into active enzymes, ultimately culminating in the formation of fibrin, the protein that physically stabilizes the blood clot. The cascade is divided into either intrinsic or extrinsic pathways that converge to activate factor X, which is a key player in the coagulation process.The intrinsic pathway is initiated by the activation of factor XII, usually by contact with subendothelial surfaces or negatively charged molecules exposed during vessel injury. This pathway involves factors XI, IX, and VIII. The extrinsic pathway is instead triggered when tissue factor (TF), a protein found on the outside of blood vessels, is exposed due to injury. TF forms a complex with factor VII, activating factor VII to its activated form, factor VIIa in the presence of calcium ions. Both intrinsic and extrinsic pathways therefore lead to the activation of factor X. The TF-factor VIIa complex cleaves and activates factor X, converting it into its active form, factor Xa. This proteolytic cleavage occurs at a specific site within the factor X molecule. Factor X then converts prothrombin (factor II) to thrombin (factor IIa) in the presence of calcium ions and phospholipids, forming a bridge between the clotting pathways. Thrombin plays a central role in coagulation. It converts fibrinogen (factor I) into fibrin, which polymerizes to form a meshwork that stabilizes the clot. Thrombin also activates platelets, amplifying their activation and promoting their aggregation. Thrombin itself is formed through positive feedback loops, ensuring a burst of thrombin generation at the site of injury. Fibrinogen is cleaved by thrombin to form fibrin monomers, which polymerize into long fibrin threads. These threads interact with platelets and other blood cells to form a stable clot that plugs the wound. Once the injury is repaired, the clotting process needs to be inhibited. Plasminogen, present in blood, is activated to plasmin by tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA). Plasmin degrades fibrin, dissolving the clot in a process termed fibrinolysis. We provide a comprehensive product range of research tools for studying blood coagulation, including Von Willebrand Factor antibodies, alpha 2 Macroglobulin antibodies, Factor XIIIa antibodies, Tissue Factor ELISA Kits, and Thrombomodulin ELISA Kits. Explore our full blood coagulation product range below and discover more, for less. Alternatively, you can explore our Regulatory, Intrinsic, and Common product ranges.