Abstract
Plasmin is the key enzyme involved in the dissolution of fibrin. It is produced from plasminogen, which is activated by a plasminogen activator -the two primary activators are tissue-type plasminogen activator (tPA) and urinary-type plasminogen activator (uPA), also called urokinase. The process is regulated by inhibitors, principally plasminogen activator inhibitor 1 (PAI-1), α2-antiplasmin (α2AP) and thrombin-activatable fibrinolysis inhibitor (TAFI). Crucial control is exerted by surfaces, such as fibrin or cells, with plasminogen activation not normally occurring in the circulation. Here we will consider the individual players of the fibrinolytic cascade and their specific locations and potential interactions. Key questions considered are the initiation of fibrinolysis and the most appropriate ways to measure abnormalities in disease situations.
Original language | English |
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Title of host publication | Trauma Induced Coagulopathy |
Editors | H.B. Moore, M.D. Neal, E.E. Moore |
Publisher | Springer |
Pages | 53-74 |
Number of pages | 22 |
ISBN (Electronic) | 9783030536060 |
ISBN (Print) | 9783030536053 |
DOIs | |
Publication status | Published - 13 Oct 2020 |
Bibliographical note
Publisher Copyright:© Springer Nature Switzerland AG 2021. All rights reserved.
Keywords
- Fibrin
- PAI-1
- Plasmin
- Plasminogen
- Platelets
- TAFI (CPB2)
- TPA
- UPA
- α2antiplasmin