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J Hepatol. 2021 Jun;74(6):1442-1454. doi: 10.1016/j.jhep.2021.02.012. Epub 2021 Feb 22.

Targeting cell-intrinsic metabolism for antifibrotic therapy.

Journal of hepatology

Helene Gilgenkrantz, Ariane Mallat, Richard Moreau, Sophie Lotersztajn

Affiliations

  1. Université de Paris, INSERM, U1149, CNRS, ERL 8252, Centre de Recherche sur l'Inflammation (CRI), Laboratoire d'Excellence Inflamex, F-75018 Paris, France.
  2. Université de Paris, INSERM, U1149, CNRS, ERL 8252, Centre de Recherche sur l'Inflammation (CRI), Laboratoire d'Excellence Inflamex, F-75018 Paris, France. Electronic address: [email protected].

PMID: 33631228 DOI: 10.1016/j.jhep.2021.02.012

Abstract

In recent years, there have been major advances in our understanding of the mechanisms underlying fibrosis progression and regression, and how coordinated interactions between parenchymal and non-parenchymal cells impact 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 the energetic and anabolic demands of phenotypic changes and effector functions. In this review, we summarise how targeting cell-intrinsic metabolic modifications of the main fibrogenic cell actors may impact on fibrosis progression and we discuss the antifibrogenic potential of metabolically targeted interventions.

Copyright © 2021 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Keywords: autophagy; fibrosis; glucose metabolism; hepatic stellate cells; hepatocytes; immunometabolism; innate-like lymphoid cells; lipid metabolism; macrophages; nuclear receptors

Conflict of interest statement

Conflict of interest The authors declare no competing financial interests. Please refer to the accompanying ICMJE disclosure forms for further details.

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