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Coagulation, Microenvironment and Liver Fibrosis

Medicina Interna, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Donato, Università Degli Studi di Milano, 20097 San Donato Milanese (MI), Italy
Fondazione IRCCS Ca’ Granda, Ospedale Maggiore Policlinico, UOC Medicina Generale-Emostasi e Trombosi, 20122 Milano, Italy
Dipartimento di Scienze biomediche per la Salute, Università degli Studi di Milano, 20122 Milano, Italy
A. M. and A. Migliavacca per lo studio delle Malattie del Fegato, 20122 Milano, Italy
Author to whom correspondence should be addressed.
Cells 2018, 7(8), 85;
Received: 10 June 2018 / Revised: 19 July 2018 / Accepted: 20 July 2018 / Published: 24 July 2018
(This article belongs to the Special Issue Extracellular Matrix Remodeling)
Fibrosis is the main consequence of any kind of chronic liver damage. Coagulation and thrombin generation are crucial in the physiological response to tissue injury; however, the inappropriate and uncontrolled activation of coagulation cascade may lead to fibrosis development due to the involvement of several cellular types and biochemical pathways in response to thrombin generation. In the liver, hepatic stellate cells and sinusoidal endothelial cells orchestrate fibrogenic response to chronic damage. Thrombin interacts with these cytotypes mainly through protease-activated receptors (PARs), which are expressed by endothelium, platelets and hepatic stellate cells. This review focuses on the impact of coagulation in liver fibrogenesis, describes receptors and pathways involved and explores the potential antifibrotic properties of drugs active in hemostasis in studies with cells, animal models of liver damage and humans. View Full-Text
Keywords: thrombin; protease-activated receptors; endothelial dysfunction; von Willebrand factor; hepatitis; cirrhosis; anticoagulation thrombin; protease-activated receptors; endothelial dysfunction; von Willebrand factor; hepatitis; cirrhosis; anticoagulation
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Bitto, N.; Liguori, E.; Mura, V.L. Coagulation, Microenvironment and Liver Fibrosis. Cells 2018, 7, 85.

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