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See: encompasses qualitative and quantitative changes in the extracellular matrix (ECM) deposits with a significant buildup of collagen-I fibers, largely produced by activated hepatic stellate cells (HSCs), which extensively distort the normal hepatic architecture.

Failure to degrade the progressive increase in scar tissue is a major reason why fibrosis evolves into cirrhosis and hepatocellular carcinoma.

Last, r HMGB1 signalled via receptor for advanced glycation end-products and activated the PI3K–p Akt1/2/3 pathway to upregulate collagen-I.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

Thus, we hypothesised that OPN by upregulating HMGB1 could participate in the pathogenesis of liver fibrosis driving scarring.

Well-established liver fibrosis along with marked induction of HMGB1 occurred in CCl-induced liver fibrosis.

Since OPN was identified as upstream of HMGB1, we hypothesised that OPN could participate in the pathogenesis of liver fibrosis by increasing HMGB1 to upregulate collagen-I expression.

Design and results Patients with long-term hepatitis C virus (HCV) progressing in disease stage displayed enhanced hepatic OPN and HMGB1 immunostaining, which correlated with fibrosis stage, whereas it remained similar in non-progressors.

Data were analysed by a two-factor analysis of variance.

All in vitro experiments were performed in triplicate at least four times. Eight mice per group were used in all the in vivo experiments, which were repeated twice.