Synonyms
Fibrinolytic defects; Abnormalities of the fibrinolytic system; Disfibrinolysis
Definition and Characteristics
Congenital or acquired abnormalities of the fibrinolytic system leading to hypo- or hyperfibrinolysis due to impaired activity of plasmin, its inhibitors, or plasminogen (PLG) activators.
Prevalence
Primary genetic disorders of fibrinolysis are uncommon, acquired fibrinolytic disorders are frequent, and secondary to other primary disorders or therapeutic interventions.
Genes
PLG coding for the plasminogen, localized or chromosome 6q26-6q27; SERPINF2 – alpha-2-plasmin inhibitor, 17p13; SERPINE1 – plasminogen activator inhibitor type 1, 7q21.3; PLAT – tissue plasminogen activator, 8p12-8p11; PLAU – urokinase-type plasminogen activator, 10q24; CPB2 – carboxypeptidase B2 (plasma) (thrombin-activatable fibrinolysis inhibitor), 13q14.1; UPAR – plasminogen activator receptor, urokinase-type (urokinase receptor), 19q13.2.
Molecular and Systemic Pathophysiology
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References
Cesarman-Maus G, Hajjar KA (2005) Molecular mechanisms of fibrinolysis. Br J Haematol 129:307–321
Schuster V, Hugle B, Tefs K (2007) Plasminogen defiency. J Thromb Haemost 5:2315–2322
Syrovets T, Simmet T (2004) Novel aspects and new roles for the serine protease plasmin. Cell Mol Life Sci 61:873–885
Longstaff C, Thelwell C (2005) Understanding the enzymology of fibrinolysis and improving thrombolytic therapy. FEBS Lett 579:3303–3309
Cale JM, Lawrence DA (2007) Structure-function relationships of plasminogen activator inhibitor-1 and its potential as a therapeutic agent. Curr Drug Targets 8:971–981
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Patrushev, L.I. (2009). Fibrinolytic Disorders. In: Lang, F. (eds) Encyclopedia of Molecular Mechanisms of Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-29676-8_636
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DOI: https://doi.org/10.1007/978-3-540-29676-8_636
Publisher Name: Springer, Berlin, Heidelberg
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