Removing plasmin from the equation - Something to chew on ...

Gael B Morrow, Nicola Mutch*

*Corresponding author for this work

Research output: Contribution to journalEditorialpeer-review

Abstract

Thrombolytics or fibrinolytics are a group of pharmacological agents used to target and dissolve occlusive intravascular thrombi. Thrombi form a haemostatic plug at the site of injury to arrest bleeding and are essential for wound healing.1 However, intravascular thrombi that aberrantly form in pathophysiological settings block blood vessels lead to disturbed blood flow, thereby promoting thromboembolic events. Degradation of a thrombus occurs when the circulating zymogen, plasminogen, is cleaved to an active serine protease, plasmin.2, 3 This process, termed fibrinolysis, is dependent on the presence of plasminogen activators; namely tissue plasminogen activator or urokinase (tPA or uPA, respectively).2, 4 The differences in the mechanism of action of tPA and uPA are also important, tPA requires fibrin as a co-factor to form a tertiary complex with plasmin,5, 6 however, uPA does not and can promote plasmin generation in solution or on the cell surface.7-9 tPA is also more susceptible to plasminogen activator inhibitor 1 (PAI-1) inhibition, as demonstrated by their second order rate constants, which differ by an order of magnitude; 12.6 × 107 vs. 4.8 × 106 M−1s−1 for tPA and uPA, respectively.10

Original languageEnglish
Pages (from-to)280-284
Number of pages5
JournalJournal of Thrombosis and Haemostasis
Volume20
Issue number2
Early online date23 Nov 2021
DOIs
Publication statusPublished - Feb 2022

Keywords

  • SINGLE-CHAIN UROKINASE
  • MOLECULAR-WEIGHT FORM
  • ACTIVATOR INHIBITOR-1
  • ISCHEMIC-STROKE
  • FIBRINOLYSIS
  • PROTEIN
  • MECHANISMS
  • ANTIBODY
  • TPA
  • ALPHA-2-ANTIPLASMIN

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