Potential Epigenetic Mechanism in Non-Alcoholic Fatty Liver Disease

被引:78
作者
Sun, Chao [1 ]
Fan, Jian-Gao [1 ]
Qiao, Liang [2 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Gastroenterol, Shanghai 200092, Peoples R China
[2] Univ Sydney, Westmead Millennium Inst Med Res, Westmead Clin Sch, Storr Liver Ctr,Westmead Hosp, Westmead, NSW 2145, Australia
基金
中国国家自然科学基金;
关键词
PROLIFERATOR-ACTIVATED RECEPTOR; ENDOPLASMIC-RETICULUM STRESS; TERM-FOLLOW-UP; HEPATIC STEATOSIS; DNA METHYLATION; INSULIN-RESISTANCE; DOWN-REGULATION; CIRCULATING MICRORNAS; URSODEOXYCHOLIC ACID; LIPID-ACCUMULATION;
D O I
10.3390/ijms16035161
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive fat accumulation in the liver. It ranges from simple steatosis to its more aggressive form, non-alcoholic steatohepatitis (NASH), which may develop into hepatic fibrosis, cirrhosis, or hepatocellular carcinoma (HCC) if it persists for a long time. However, the exact pathogenesis of NAFLD and the related metabolic disorders remain unclear. Epigenetic changes are stable alterations that take place at the transcriptional level without altering the underlying DNA sequence. DNA methylation, histone modifications and microRNA are among the most common forms of epigenetic modification. Epigenetic alterations are involved in the regulation of hepatic lipid metabolism, insulin resistance, mitochondrial damage, oxidative stress response, and the release of inflammatory cytokines, all of which have been implicated in the development and progression of NAFLD. This review summarizes the current advances in the potential epigenetic mechanism of NAFLD. Elucidation of epigenetic factors may facilitate the identification of early diagnositic biomarkers and development of therapeutic strategies for NAFLD.
引用
收藏
页码:5161 / 5179
页数:19
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