Abstract
Nonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide in part due to the concomitant obesity pandemic and insulin resistance (IR). It is increasingly becoming evident that NAFLD is a disease affecting numerous extrahepatic vital organs and regulatory pathways. The molecular mechanisms underlying the nonalcoholic steatosis formation are poorly understood, and little information is available on the pathways that are responsible for the progressive hepatocellular damage that follows lipid accumulation. Recently, much research has focused on the identification of the epigenetic modifications that contribute to NAFLD pathogenesis. Noncoding RNAs (ncRNAs) are one of such epigenetic factors that could be implicated in the NAFLD development and progression. In this review, we summarize the current knowledge of the genetic and epigenetic factors potentially underlying the disease. Particular emphasis will be put on the contribution of microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs) to the pathophysiology of NAFLD as well as their potential use as therapeutic targets or as markers for the prediction and the progression of the disease.
Highlights
Nonalcoholic fatty liver disease is the accumulation of lipids in the liver above 5% of the total liver weight, in the absence of other medical conditions
Some 20% of individuals with nonalcoholic steatohepatitis (NASH) will progress to fibrosis, a stage characterized by the scarring of the liver [7]
These findings uncover a new mechanism for epigenetic modification in liver fibrogenesis, which involves the interaction between two different long noncoding RNAs (lncRNAs) (HOTAIR and MEG3) [76]
Summary
Nonalcoholic fatty liver disease is the accumulation of lipids in the liver above 5% of the total liver weight, in the absence of other medical conditions It is currently the most common chronic liver disease worldwide, with a global prevalence of around 25% [1]. In advanced NAFLD, impairment of mitochondrial β-oxidation aggravates the hepatic accumulation of lipid products. In concert with the extrahepatic glucose, which is augmented due to peripheral IR, the glucose from hepatic origin stimulates de novo lipogenesis [18]. All these events are intertwined, and vicious cycles can arise between them
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