Gilgenkrantz Helene, Mallat Ariane, Moreau Richard, Lotersztajn Sophie
Université de Paris, INSERM, U1149, CNRS, ERL 8252, Centre de Recherche sur l'Inflammation (CRI), Laboratoire d'Excellence Inflamex, F-75018 Paris, France.
Université de Paris, INSERM, U1149, CNRS, ERL 8252, Centre de Recherche sur l'Inflammation (CRI), Laboratoire d'Excellence Inflamex, F-75018 Paris, France.
J Hepatol. 2021 Jun;74(6):1442-1454. doi: 10.1016/j.jhep.2021.02.012. Epub 2021 Feb 22.
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.
近年来，我们对纤维化进展和消退的潜在机制，以及实质细胞和非实质细胞之间的协同相互作用如何影响纤维化过程的理解取得了重大进展。最近的研究强调，实质细胞、免疫细胞（免疫代谢）和肝星状细胞的代谢重编程是支持表型变化和效应器功能的能量和合成代谢需求所必需的。在这篇综述中，我们总结了针对主要纤维化细胞的细胞内在代谢修饰如何可能影响纤维化进展，并讨论了代谢靶向干预的抗纤维化潜力。
