Semin Thromb Hemost 2024; 50(04): 638-647
DOI: 10.1055/s-0044-1779738
Review Article

Fibrinolysis-Mediated Pathways in Acute Liver Injury

Gina E. Capece
1   Department of Pharmacology, Rutgers University Robert Wood Johnson Medical School, Piscataway, New Jersey
,
James P. Luyendyk
2   Department of Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, Michigan
,
Lauren G. Poole
1   Department of Pharmacology, Rutgers University Robert Wood Johnson Medical School, Piscataway, New Jersey
› Author Affiliations

Funding J.P.L. and L.G.P. received funding from the National Institutes of Health to support this work. Funding support from the National Institutes of Health (R01 DK135649 to JPL, and P30 ES005022 and R00 DK129710 to LGP) and training support from the Grover Fellowship to GC are gratefully acknowledged.
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Abstract

Acute liver injury (ALI), that is, the development of reduced liver function in patients without preexisting liver disease, can result from a wide range of causes, such as viral or bacterial infection, autoimmune disease, or adverse reaction to prescription and over-the-counter medications. ALI patients present with a complex coagulopathy, characterized by both hypercoagulable and hypocoagulable features. Similarly, ALI patients display a profound dysregulation of the fibrinolytic system with the vast majority of patients presenting with a hypofibrinolytic phenotype. Decades of research in experimental acute liver injury in mice suggest that fibrinolytic proteins, including plasmin(ogen), plasminogen activators, fibrinolysis inhibitors, and fibrin(ogen), can contribute to initial hepatotoxicity and/or stimulate liver repair. This review summarizes major experimental findings regarding the role of fibrinolytic factors in ALI from the last approximately 30 years and identifies unanswered questions, as well as highlighting areas for future research.



Publication History

Article published online:
23 February 2024

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