%0 Journal Article
%T Coagulation Factor XIII in Cerebral Venous Thrombosis
%A Bojun Li
%A Hans P. Kohler
%A Jonathan M. Coutinho
%A Joost C. M. Meijers
%A Marcel Arnold
%A Mirjam R. Heldner
%A Susanna M. Zuurbier
%A Verena Schroeder
%J Archive of "TH Open: Companion Journal to Thrombosis and Haemostasis".
%D 2019
%R 10.1055/s-0039-1693487
%X Coagulation factor XIII (FXIII) is activated in the last stage of the coagulation cascade in the presence of thrombin and Ca 2+ by cleavage and release of the activation peptide (FXIII activation peptide, AP-FXIII) from the A-subunit and dissociation of the carrier B-subunits. Activated FXIII then crosslinks fibrin fibers and incorporates antifibrinolytic proteins into the clot. Therefore, FXIII has a crucial role in stabilizing fibrin: it determines clot properties and fibrinolysis, and contributes to clot formation in every acute thrombotic event. 1 Consequently, FXIII is consumed during acute thrombotic events leading to a reduction in systemic circulating FXIII plasma levels which are also associated with outcome, e.g., in acute myocardial infarction, 2 stroke, 3 4 5 and venous thromboembolism. 6 7 8 9 In patients with acute stroke, we could detect circulating free AP-FXIII for the first time and prove its release during an acute thrombotic event. 4 1
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6645911/