Mitochondria in non-alcoholic fatty liver disease

Int J Biochem Cell Biol. 2018 Feb;95:93-99. doi: 10.1016/j.biocel.2017.12.019. Epub 2017 Dec 26.

Abstract

NAFLD is a common disease in Western society and ranges from steatosis to steatohepatitis and to end-stage liver disease. The molecular mechanisms that cause the progression of steatosis to severe liver damage are not fully understood. One suggested mechanism involves the oxidation of biomolecules by mitochondrial ROS which initiates a vicious cycle of exacerbated mitochondrial dysfunction and increased hepatocellular oxidative damage. This may ultimately pave the way for hepatic inflammation and liver failure. This review updates our current understanding of mitochondria-derived oxidative stress in the progression of NAFLD.

Keywords: Mitochondria; NAFLD; NASH; ROS; Steatosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Disease Progression
  • End Stage Liver Disease / etiology
  • Humans
  • Mitochondria, Liver / immunology
  • Mitochondria, Liver / metabolism*
  • Mitochondria, Liver / pathology
  • Non-alcoholic Fatty Liver Disease / immunology
  • Non-alcoholic Fatty Liver Disease / metabolism*
  • Non-alcoholic Fatty Liver Disease / pathology
  • Non-alcoholic Fatty Liver Disease / physiopathology
  • Oxidation-Reduction
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism*
  • Severity of Illness Index

Substances

  • Reactive Oxygen Species