scholarly journals Hepatic Fibrosis Is Enhanced and Accompanied by Robust Oval Cell Activation after Chronic Carbon Tetrachloride Administration to Egr-1-Deficient Mice

2010 ◽  
Vol 176 (6) ◽  
pp. 2743-2752 ◽  
Author(s):  
Michele T. Pritchard ◽  
Laura E. Nagy
Keyword(s):  
Carbon Tetrachloride ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Oval Cell ◽  
Carbon Tetrachloride Administration ◽  
Deficient Mice

scholarly journals Selenium Supplementation Decreases Hepatic Fibrosis in Mice After Chronic Carbon Tetrachloride Administration

2009 ◽  
Vol 133 (1) ◽  
pp. 83-97 ◽  
Author(s):  
Ming Ding ◽  
James J. Potter ◽  
Xiaopu Liu ◽  
Michael S. Torbenson ◽  
Esteban Mezey
Keyword(s):  
Carbon Tetrachloride ◽  
Hepatic Fibrosis ◽  
Selenium Supplementation ◽  
Carbon Tetrachloride Administration

Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell
Keyword(s):  
Wound Healing ◽  
Liver Disease ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Factor Xa ◽  
Clinical Trial Data ◽  
Chronic Liver ◽  
Healing Response ◽  
Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

RAGE is required for oval cell activation and inflammation-associated mouse liver carcinogenesis

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
T Pusterla ◽  
J Németh ◽  
I Stein ◽  
L Wiechert ◽  
D Knigin ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Cell Activation ◽  
Oval Cell ◽  
Liver Carcinogenesis

scholarly journals Hepatoprotective effect of Matrine salvianolic acid B salt on Carbon Tetrachloride-Induced Hepatic Fibrosis

2012 ◽  
Vol 9 (1) ◽  
pp. 16 ◽  
Author(s):  
Hong-Ying Gao ◽  
Guo-Yu Li ◽  
Meng-Meng Lou ◽  
Xiao-Yu Li ◽  
Xiu-Yan Wei ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Hepatic Fibrosis ◽  
Salvianolic Acid B ◽  
Hepatoprotective Effect ◽  
Salvianolic Acid
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