Redox Homeostasis and Epigenetics in Non-alcoholic Fatty Liver Disease (NAFLD)
Christine Podrini, Michela Borghesan, Azzura Greco, Valerio Pazienza, Gianluigi Mazzoccoli and Manlio Vinciguerra
Affiliation: The Institute of Hepatology, The Foundation for Liver Research, 69-75 Chenies Mews, London, WC1E 6HX, United Kingdom.
Non-alcoholic fatty liver disease (NAFLD), an accumulation of intra-hepatic triglycerides that is often considered the hepatic
manifestation of insulin resistance, is the most common cause of chronic liver disease in the Western countries with up to one third of the
population affected. NAFLD is a spectrum of disturbances that encompasses various degrees of liver damage ranging from simple steatosis
to non-alcoholic steatohepatitis (NASH). NASH is characterized by hepatocellular injury/inflammation with or without fibrosis. The
individuals with NAFLD develop NASH in 10% of the cases, and are also at risk of developing hepatocellular carcinoma (HCC). Epigenetic
mechanisms of nuclear chromatin remodeling, such as DNA methylation, post-translational modifications of histones, and incorporation
of histone variants into the chromatin are increasingly recognized as crucial factors in the pathophysiology of NAFLD. NAFLD is
often accompanied by oxidative stress: reactive oxygen species (ROS) are implicated in altered reduction/oxidation (redox) reactions that
attack cellular macromolecules and are detected in the liver of patients and animal models of NAFLD. In this review, we summarize recent
knowledge advancements in the hepatic epigenetic and redox mechanisms, and their possible links, involved in the pathogenesis and
treatment of NAFLD.
Keywords: Non-alcoholic fatty liver disease (NAFLD), epigenetics, oxidative stress
Rights & PermissionsPrintExport