LAUSR

In recent years, major advances have been made regarding our understanding on the mechanisms underlying fibrosis progression and regression, and on how coordinated dialog between parenchymal and non-parenchymal cells impacts on the fibrogenic process. Recent studies have highlighted that metabolic reprogramming of parenchymal cells, immune cells (immunometabolism) and hepatic stellate cells is required to support their energy and anabolic demands for acquisition and/or changes in their phenotype and effector functions. In this review, we summarize the current knowledge on how targeting cell-intrinsic metabolic modifications of the main fibrogenic cell actors may impact on fibrosis progression and discuss the anti-fibrogenic potential of metabolically-targeted interventions.