Abstract
The end-product of coagulation is a clot with a fibrin meshwork. Fibrin, however, is not a permanent structure, but stimulates a biochemical pathway that leads to its lysis pathway and fragmentation of the clot. Essential components of this, as a consequence, are the plasminogen activators (PAs). PAs convert the zymogen plasminogen to the ultimate fibrinolytic enzyme plasmin (Fig. 1). At least two types of PAs have been identified in plasma: one produced and secreted by endothelial cells (first isolated in urine), called tissue-type PA (t-PA), and another called urinary-type PA or urokinase (UK). UK was later also identified in plasma, mainly as a proenzyme known as pro-urokinase (pro-UK). t-PA and pro-UK both activate plasminogen, preferentially in the presence of fibrin, but by different mechanisms (for review, see [5]).
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Andreotti, F., Davies, G.J., Maseri, A., Kluft, C. (1989). Inhibition of fibrinolysis in blood: circadian fluctuation and possible relevance to coronary artery disease. In: v. Arnim, T., Maseri, A. (eds) Predisposing Conditions for Acute Ischemic Syndromes. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-662-09434-1_3
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DOI: https://doi.org/10.1007/978-3-662-09434-1_3
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