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.
Coagulation, Microenvironment and Liver Fibrosis / N. Bitto, E. Liguori, V. La Mura. - In: CELLS. - ISSN 2073-4409. - 7:8(2018 Jul), pp. 85.1-85.19.
|Titolo:||Coagulation, Microenvironment and Liver Fibrosis|
BITTO, NICCOLO (Primo)
LIGUORI, ELEONORA (Secondo)
LA MURA, VINCENZO (Ultimo) [Conceptualization] (Corresponding)
|Parole Chiave:||anticoagulation; cirrhosis; endothelial dysfunction; hepatitis; protease-activated receptors; thrombin; von Willebrand factor|
|Settore Scientifico Disciplinare:||Settore MED/09 - Medicina Interna|
Settore MED/12 - Gastroenterologia
Settore MED/17 - Malattie Infettive
Settore MED/15 - Malattie del Sangue
|Data di pubblicazione:||lug-2018|
|Digital Object Identifier (DOI):||http://dx.doi.org/10.3390/cells7080085|
|Appare nelle tipologie:||01 - Articolo su periodico|