The Role of Epigenetics in the Progression of Non-Alcoholic Fatty Liver Disease

被引:6
|
作者
Edith Aguilar-Olivos, Nancy [1 ]
Oria-Hernandez, Jesus [2 ]
Ponciano-Rodriguez, Guadalupe [3 ]
Carlos Chavez-Tapia, Norberto [4 ]
Uribe, Misael [4 ]
Mendez-Sanchez, Nahum [1 ]
机构
[1] Medica Sur Clin & Fdn, Liver Res Unit, Mexico City 14050, DF, Mexico
[2] Minist Hlth, Natl Inst Pediat, Biochem & Genet Lab, Mexico City, DF, Mexico
[3] Univ Nacl Autonoma Mexico, Fac Med, Dept Publ Hlth, Mexico City 04510, DF, Mexico
[4] Medica Sur Clin & Fdn, Obes & Digest Dis Unit, Mexico City 14050, DF, Mexico
关键词
Biological markers; disease progression; DNA methylation; histones; liver; microRNAs; one-carbon metabolism; NICOTINAMIDE-N-METHYLTRANSFERASE; ATP-CITRATE LYASE; INSULIN-RESISTANCE; HEPATIC STEATOSIS; SIRT1; STEATOHEPATITIS; METABOLISM; MICE; METHYLATION; MICRORNAS;
D O I
10.2174/1389557515666150709115702
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Non-alcoholic fatty liver disease encompasses a spectrum of pathologies ranging from simple steatosis to non-alcoholic steatohepatitis. Patients with non-alcoholic steatohepatitis have increased risk of cirrhosis, liver failure and hepatocellular carcinoma. About 25% of subjects with simple steatosis progress to steatohepatitis; nowadays, the detailed pathological factors influencing the progression of non-alcoholic fatty liver disease remains unclear. It is proposed that genetic and environmental factors interact to determine the disease phenotype. Epigenetics could explain some relationships between genes and external influences. The epigenetic changes that have been related to non-alcoholic fatty liver disease are DNA methylation, one-carbon metabolism, histone modifications and the presence of micro-RNA. DNA methylation and micro-RNAs have been investigated in human samples, whereas histone modifications have only been studied until now in animal and cellular models. The aim of this study is to review the most relevant information about epigenetic changes in non-alcoholic steatohepatitis.
引用
收藏
页码:1187 / 1194
页数:8
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