3 Citations (Scopus)


The pathogenesis of nonalcoholic fatty liver disease (NAFLD) is multifactorial and difficult to unify. The progression of benign nonalcoholic fatty liver (NAFL) to progressive nonalcoholic steatohepatitis (NASH) is acknowledged to be a multiple parallel hit process. Oxidative stress is one of the main factors that drives progression of NAFL to NASH, although it is also essential for vital cellular processes. Overaccumulation of long chain fatty acid results in mitochondrial ?-oxidation pathway activation followed by reactive oxygen species (ROS) production. ROS can mediate the oxidative stress response in hepatocytes, Kupffer cells, or hepatic stellate cells resulting in hepatocyte damage, and in proinflammatory and profibrogenic responses that should be well balanced. ROS detoxification pathway signaling is often damaged in NAFLD following ROS accumulation. Inactivation of pro-oxidant production pathways and activation of detoxifying signaling pathways are the required treatment approach.

Original languageEnglish
Title of host publicationLiver Pathophysiology
Subtitle of host publicationTherapies and Antioxidants
Number of pages12
ISBN (Electronic)9780128043219
ISBN (Print)9780128042748
Publication statusPublished - Mar 23 2017


  • Genome-wide association study
  • Hepatocellular carcinoma
  • Nonalcoholic fatty liver disease
  • Nonalcoholic steatohepatitis
  • Reactive oxygen species
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Medicine(all)


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