Targeting cell-intrinsic metabolism for antifibrotic therapy

JOURNAL OF HEPATOLOGY

卷:74

Review

Gilgenkrantz, Helene¹  Mallat, Ariane¹  Moreau, Richard¹  Lotersztajn, Sophie¹ 

[1] Univ Paris, Ctr Rech Inflammat CRI, Lab Excellence Inflamex, INSERM,U1149,CNRS,ERL 8252, F-75018 Paris, France

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

DOI  :  10.1016/j.jhep.2021.02.012

来源: Elsevier

【 摘 要 】

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. (C) 2021 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

【 授权许可】

Free