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Epigenetic Mechanisms in Hepatic Stellate Cell Activation During Liver Fibrosis and Carcinogenesis

1
Hepatology Program, CIMA, University of Navarra, 31180 Pamplona, Spain
2
CIBERehd, Instituto de Salud Carlos III, 28029 Madrid, Spain
3
Instituto de Investigaciones Sanitarias de Navarra-IdiSNA, 31180 Pamplona, Spain
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(10), 2507; https://doi.org/10.3390/ijms20102507
Received: 29 April 2019 / Revised: 17 May 2019 / Accepted: 19 May 2019 / Published: 21 May 2019
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. View Full-Text
Keywords: Tumor microenvironment; fibrosis; hepatic stellate cells; epigenetic remodeling Tumor microenvironment; fibrosis; hepatic stellate cells; epigenetic remodeling
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MDPI and ACS Style

Barcena-Varela, M.; Colyn, L.; Fernandez-Barrena, M.G. Epigenetic Mechanisms in Hepatic Stellate Cell Activation During Liver Fibrosis and Carcinogenesis. Int. J. Mol. Sci. 2019, 20, 2507.

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