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Updated: Feb 7, 2026

Assessment of Plasma Coagulation on Liver Tissue in a Large Animal Model In Vivo
Published on: August 4, 2018
Coagulation, Microenvironment and Liver Fibrosis
Niccolò Bitto1, Eleonora Liguori2, Vincenzo La Mura3,4,5
1Medicina Interna, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Donato, Università Degli Studi di Milano, 20097 San Donato Milanese (MI), Italy. nicobitto@gmail.com.
Uncontrolled blood clotting (coagulation) and thrombin generation contribute to liver fibrosis. Targeting coagulation pathways may offer new antifibrotic therapies for chronic liver damage.
Area of Science:
- Hepatology
- Hematology
- Cellular Biology
Background:
- Fibrosis is a common outcome of chronic liver injury.
- Aberrant coagulation and thrombin generation are implicated in fibrogenesis.
- Hepatic stellate cells and sinusoidal endothelial cells are key players in liver fibrotic responses.
Purpose of the Study:
- To review the role of coagulation in liver fibrogenesis.
- To describe the receptors and pathways involved in thrombin-mediated liver damage.
- To explore potential antifibrotic effects of hemostasis-modulating drugs.
Main Methods:
- Literature review focusing on coagulation and liver fibrosis.
- Analysis of cellular and molecular mechanisms involving thrombin and protease-activated receptors (PARs).
- Examination of studies involving cell cultures, animal models, and human subjects.
Main Results:
- Thrombin, via PARs on hepatic stellate cells and endothelial cells, drives fibrogenic pathways.
- Uncontrolled coagulation activation exacerbates liver damage and promotes fibrosis.
- Evidence suggests drugs affecting hemostasis may possess antifibrotic properties.
Conclusions:
- Coagulation plays a significant role in the development of liver fibrosis.
- Targeting thrombin generation and its receptors presents a potential therapeutic strategy.
- Further research into hemostasis-modulating drugs could yield novel antifibrotic treatments for liver diseases.
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