Epigenetic mechanisms in hepatic stellate cell activation during liver fibrosis and carcinogenesis
Keywords: 
Tumor microenvironment
Fibrosis
Hepatic stellate cells
Epigenetic remodeling
Issue Date: 
2019
Publisher: 
MDPI AG
ISSN: 
1422-0067
Note: 
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Citation: 
Bárcena-Varela, M. (Marina); Colyn, L. (Leticia); García-Fernández-de-Barrena, M. (Maite). "Epigenetic mechanisms in hepatic stellate cell activation during liver fibrosis and carcinogenesis". International Journal of Molecular Sciences. 20 (10), 2019, 2507
Abstract
Liver fibrosis is an essential component of chronic liver disease (CLD) and hepatocarcinogenesis. The fibrotic stroma is a consequence of sustained liver damage combined with exacerbated extracellular matrix (ECM) accumulation. In this context, activation of hepatic stellate cells (HSCs) plays a key role in both initiation and perpetuation of fibrogenesis. These cells suffer profound remodeling of gene expression in this process. This review is focused on the epigenetic alterations participating in the transdifferentiation of HSCs from the quiescent to activated state. Recent advances in the field of DNA methylation and post-translational modifications (PTM) of histones (acetylation and methylation) patterns are discussed here, together with altered expression and activity of epigenetic remodelers. We also consider recent advances in translational approaches, including the use of epigenetic marks as biomarkers and the promising antifibrotic properties of epigenetic drugs that are currently being used in patients.

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