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Blood Rev. 2015 Jan;29(1):17-24. doi: 10.1016/j.blre.2014.09.003. Epub 2014 Sep 16.

Fibrinolysis and the control of blood coagulation.

Author information

1
Division of Hematology-Oncology, Department of Medicine, Weill Cornell Medical College, 520 East 70th Street, New York, NY 10065, USA. Electronic address: joc9160@med.cornell.edu.
2
Division of Hematology-Oncology, Department of Medicine, Weill Cornell Medical College, 520 East 70th Street, New York, NY 10065, USA; Division of Hematology-Oncology, Department of Pediatrics, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA; Department of Cell and Developmental Biology, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA. Electronic address: khajjar@med.cornell.edu.

Abstract

Fibrin plays an essential role in hemostasis as both the primary product of the coagulation cascade and the ultimate substrate for fibrinolysis. Fibrinolysis efficiency is greatly influenced by clot structure, fibrinogen isoforms and polymorphisms, the rate of thrombin generation, the reactivity of thrombus-associated cells such as platelets, and the overall biochemical environment. Regulation of the fibrinolytic system, like that of the coagulation cascade, is accomplished by a wide array of cofactors, receptors, and inhibitors. Fibrinolytic activity can be generated either on the surface of a fibrin-containing thrombus, or on cells that express profibrinolytic receptors. In a widening spectrum of clinical disorders, acquired and congenital defects in fibrinolysis contribute to disease morbidity, and new assays of global fibrinolysis now have potential predictive value in multiple clinical settings. Here, we summarize the basic elements of the fibrinolytic system, points of interaction with the coagulation pathway, and some recent clinical advances.

KEYWORDS:

Coagulation; Fibrin(ogen); Fibrinolysis; Hemostasis; Thrombosis

PMID:
25294122
PMCID:
PMC4314363
DOI:
10.1016/j.blre.2014.09.003
[Indexed for MEDLINE]
Free PMC Article

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