Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10815422 | Cellular Signalling | 2013 | 8 Pages |
Abstract
Epigenetics refers to the study of heritable changes in the pattern of gene expression that is controlled by a mechanism specifically not due to changes the primary DNA sequence. Well-known epigenetic mechanisms include DNA methylation, post-translational histone modifications and RNA-based mechanisms including those controlled by small non-coding RNAs (miRNAs). Recent studies have shown that epigenetic modifications orchestrate the hepatic stellate cell (HSC) activation and liver fibrosis. In this review we focus on the aberrant methylation of CpG island promoters of select genes is the prominent epigenetic mechanism to effectively silence gene transcription facilitating HSC activation and liver fibrosis. Furthermore, we also discuss epigenetic dysregulation of tumor-suppressor miRNA genes by promoter DNA methylation and the interaction of DNA methylation with miRNAs involved in the regulation of HSC activation and liver fibrosis. Recent advances in epigenetics alterations in the pathogenesis of liver fibrosis and their possible use as new therapeutic targets and biomarkers.
Keywords
GLI1IUGRTGF-βMecp2MBDmethyl-CpG-binding domainRASAL1PDGFCDH1ECMTDGDNMTsTSGPTCH1Patched1DNA methyltransferasesGSTP1pri-miRNAsTETPI3Kα-SMAHSCmiRNAsUTRBERICAM-1FGFglutathione S-transferase Pi 1PPARγMCP-15-Aza-2′-deoxycytidineBDNFThymine DNA glycosylaseNFκBRBPsSmall non-coding RNAsα-smooth muscle actintransforming growth factor-βbase excision repairHepatic stellate cellplatelet-derived growth factorfibroblast growth factorBrain-derived neurotrophic factornuclear factor κBphosphatidylinositol-3-kinaseLiver fibrosisExtracellular matrixDNA methylationintrauterine growth restrictionuntranslated regionintercellular adhesion molecule-1MicroRNAPhosphatase and tensin homologueglioma-associated oncogene homolog 1Monocyte chemotactic protein-1RNA-binding proteinsPtentumor-suppressor gene
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Authors
Er-Bao Bian, Bing Zhao, Cheng Huang, Hua Wang, Xiao-Ming Meng, Bao-Ming Wu, Tao-Tao Ma, Lei Zhang, Xiong-Wen Lv, Jun Li,