Liver fibrosis is an important pathological repair process in reaction to liver injury characterized by progressive accumulation of extracellular matrix (ECM) components. Mechanism that orchestrates this fibrotic disorder is the activation of hepatic stellate cell (HSC) that requires extensive alterations in gene expression. Reversible deacetylation of histone proteins is one of the most abundant epigenetic modifications and is crucial in modulating gene expression. Recent evidence has highlighted a pathological imbalance between the acetylation and deacetylation of histone proteins regulated by histone deacetylases (HDACs). In the past several years, the role of HDACs in liver fibrosis initiation and progression, as well as the therapeutic effects of HDAC inhibitors, has been well studied. Here, the innovative aspects of histone deacetylation will be presented, with respect to the roles of HDACs in liver fibrosis, the affected genes and signal pathways involved in HSCs activation, as well as significant data emerging from the field in support of HDAC inhibitors as potential therapeutic targets for the treatment of liver fibrosis.
Keywords: HDAC inhibitors; Hepatic stellate cell; Histone deacetylases; Liver fibrosis.
Copyright © 2015. Published by Elsevier B.V.