Endoglin Upregulation in the Liver after Bile Duct Ligation in Rats

Pérez‐Barriocanal, Fernando

doi:10.2174/1874259901105010001

Cited by 2 publications

(2 citation statements)

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“…A recent study by another group reported a similar increase in endoglin expression in the liver following bile duct ligation in rats, but transfection of human endoglin did not alter liver fibrosis (Pérez‐Barriocanal et al 2011). These findings suggest that generalized overexpression of endoglin in the liver may not alter the fibrotic process in the liver.…”

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confidence: 86%

Endoglin in liver fibrosis

Finnson

Philip

2011

J. Cell Commun. Signal.

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Liver fibrosis occurs in most types of chronic liver diseases and is characterized by excessive accumulation of extracellular matrix proteins, leading to disruption of tissue function and eventually organ failure. Transforming growth factor (TGF)‐β represents an important pro‐fibrogenic factor and aberrant TGF‐β action has been implicated in many disease processes of the liver. Endoglin is a TGF‐β co‐receptor expressed mainly in endothelial cells that has been shown to differentially regulates TGF‐β signal transduction by inhibiting ALK5‐Smad2/3 signalling and augmenting ALK1‐Smad1/5 signalling. Recent reports demonstrating upregulation of endoglin expression in pro‐fibrogenic cell types such as scleroderma fibroblasts and hepatic stellate cells have led to studies exploring the potential involvement of this TGF‐β co‐receptor in organ fibrosis. A recent article by Meurer and colleagues now shows that endoglin expression is increased in transdifferentiating hepatic stellate cells in vitro and in two different models (carbon tetrachloride intoxication and bile duct ligation) of liver fibrosis in vivo. Moreover, they show that endoglin overexpression in hepatic stellate cells is associated with enhanced TGF‐β‐driven Smad1/5 phosphorylation and α‐smooth muscle actin production without altering Smad2/3 signaling. These findings suggest that endoglin may play an important role in hepatic fibrosis by altering the balance of TGF‐β signaling via the ALK1‐Smad1/5 and ALK‐Smad2/3 pathways and raise the possibility that targeting endoglin expression in transdifferentiating hepatic stellate cells may represent a novel therapeutic strategy for the treatment of liver fibrosis.

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