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A mathematical model of plasmin-mediated fibrinolysis of single fibrin fibers.
PLoS Comput Biol
December 2024
Department of Mathematics and Statistics, University of Central Oklahoma, Edmond, Oklahoma, United States of America.
Fibrinolysis, the plasmin-mediated degradation of the fibrin mesh that stabilizes blood clots, is an important physiological process, and understanding mechanisms underlying lysis is critical for improved stroke treatment. Experimentalists are now able to study lysis on the scale of single fibrin fibers, but mathematical models of lysis continue to focus mostly on fibrin network degradation. Experiments have shown that while some degradation occurs along the length of a fiber, ultimately the fiber is cleaved at a single location.
View Article and Find Full Text PDFDependence of clot structure and fibrinolysis on apixaban and clotting activator.
Res Pract Thromb Haemost
November 2024
Department of Biomedical Engineering, Rutgers University, Piscataway, New Jersey, USA.
Background: Anticoagulants prevent the formation of potentially fatal blood clots. Apixaban is a direct oral anticoagulant that inhibits factor (F)Xa, thereby impeding the conversion of prothrombin into thrombin and the formation of blood clots. Blood clots are held together by fibrin networks that must be broken down (fibrinolysis) to restore blood flow.
View Article and Find Full Text PDFEnhanced thrombin and plasmin generation profiles in alpha-2-antiplasmin-deficient patients: Data from the Rare Bleeding disorders in the Netherlands study.
Res Pract Thromb Haemost
October 2024
Department of Hematology, Radboud University Medical Center, Nijmegen, the Netherlands.
Background: α2-Antiplasmin (A2AP) deficiency is a rare and often unidentified disorder characterized by increased fibrinolysis and subsequent bleeding. Global hemostasis assays may increase insight into the altered coagulation and fibrinolysis in these patients.
Objectives: To explore thrombin and plasmin generation profiles in A2AP-deficient patients, corresponding A2AP activity levels and associated bleeding phenotypes.
Use of Affimer technology for inhibition of α2-antiplasmin and enhancement of fibrinolysis.
Blood Adv
January 2025
Discovery and Translational Science Department, Leeds Institute for Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, Leeds, United Kingdom.
Hypofibrinolysis is a documented abnormality in conditions with high risk of vascular occlusion. A key inhibitor of fibrinolysis is α2-antiplasmin (α2AP), and we hypothesize that the Affimer technology, comprising small conformational proteins with 2 9-amino-acid variable regions, can be used to modulate α2AP activity and facilitate fibrinolysis. Using a phage display system, a library of Affimers was screened against α2AP.
View Article and Find Full Text PDFHyperfibrinolysis: a crucial phenotypic abnormality of posttraumatic fibrinolytic dysfunction.
Res Pract Thromb Haemost
October 2024
Division of Acute Care Surgery, University of Southern California, Los Angeles, California, USA.
Background: Traumatic fibrinolytic dysfunction is often categorized into 3 phenotypes based on the result of thromboelastography (TEG) lysis at 30 minutes (LY30): fibrinolysis shutdown, physiologic fibrinolysis, and hyperfibrinolysis. However, the molecular pathophysiology of fibrinolytic dysfunction and the association with clinical outcomes have not been fully evaluated.
Objectives: To assess whether posttraumatic fibrinolysis phenotypes identified by TEG correlate with levels of key fibrinolysis-related serum markers and with risk of mortality and hospital complications.
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