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© Research
Publication : Scientific reports

Hepatic stellate cell hypertrophy is associated with metabolic liver fibrosis

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Scientific reports - 02 Mar 2020

Hoffmann C, Djerir NEH, Danckaert A, Fernandes J, Roux P, Charrueau C, Lachagès AM, Charlotte F, Brocheriou I, Clément K, Aron-Wisnewsky J, Foufelle F, Ratziu V, Hainque B, Bonnefont-Rousselot D, Bigey P, Escriou V

Link to Pubmed [PMID] – 32123215

Sci Rep 2020 Mar;10(1):3850

Hepatic fibrosis is a major consequence of chronic liver disease such as non-alcoholic steatohepatitis which is undergoing a dramatic evolution given the obesity progression worldwide, and has no treatment to date. Hepatic stellate cells (HSCs) play a key role in the fibrosis process, because in chronic liver damage, they transdifferentiate from a “quiescent” to an “activated” phenotype responsible for most the collagen deposition in liver tissue. Here, using a diet-induced liver fibrosis murine model (choline-deficient amino acid-defined, high fat diet), we characterized a specific population of HSCs organized as clusters presenting simultaneously hypertrophy of retinoid droplets, quiescent and activated HSC markers. We showed that hypertrophied HSCs co-localized with fibrosis areas in space and time. Importantly, we reported the existence of this phenotype and its association with collagen deposition in three other mouse fibrosis models, including CCl-induced fibrosis model. Moreover, we have also shown its relevance in human liver fibrosis associated with different etiologies (obesity, non-alcoholic steatohepatitis, viral hepatitis C and alcoholism). In particular, we have demonstrated a significant positive correlation between the stage of liver fibrosis and HSC hypertrophy in a cohort of obese patients with hepatic fibrosis. These results lead us to conclude that hypertrophied HSCs are closely associated with hepatic fibrosis in a metabolic disease context and may represent a new marker of metabolic liver disease progression.

https://www.ncbi.nlm.nih.gov/pubmed/32123215