DNA methylation: New therapeutic implications for hepatic fibrosis

被引：26

作者：

Bian, Er-Bao ^{[1
]}

Huang, Cheng ^{[1
]}

Wang, Hua ^{[1
]}

Wu, Bao-Ming ^{[1
]}

Zhang, Lei ^{[1
]}

Lv, Xiong-wen ^{[1
]}

Li, Jun ^{[1
]}

机构：

[1] Anhui Med Univ, Sch Pharm, Hefei 230032, Anhui, Peoples R China

来源：

CELLULAR SIGNALLING | 2013年 / 25卷 / 01期

基金：

美国国家科学基金会;

关键词：

Liver fibrosis; Hepatic stellate cell; DNA methylation; Signaling pathway; STELLATE CELL ACTIVATION; TGF-BETA; SIGNALING PATHWAYS; GENE-EXPRESSION; LIVER FIBROSIS; CANCER-THERAPY; FIBROGENESIS; DNMT1; PROTEIN; MECP2;

D O I：

10.1016/j.cellsig.2012.10.007

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

DNA methylation refers to a heritable alteration in the pattern of gene expression that is regulated by a mechanism specifically not owing to changes in the primary nucleotide sequence. The transcriptional silencing caused by DNA methylation affects genes involved in the main cellular pathways: cell cycle control. Ras signaling, apoptosis, and detoxification. Recent studies have shown that methylation modifications orchestrate the activation of hepatic stellate cells (HSCs) characterized by excessive accumulation of extracellular matrices (ECMs). The activation of HSCs is mediated by multiple signal transduction pathways and is generally regarded as the major ECM producer responsible for liver fibrosis. In addition, aberrant methylation of specific gene involved in the activation of multiple signal transduction pathways in liver fibrosis. The aim of this review is to compile recent information on aberrant DNA methylation in hepatic fibrosis and to highlight key genes and molecular pathways in hepatic fibrosis formation. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：355 / 358

页数：4

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