title: Oxidative Stress as a Critical Factor in Nonalcoholic Fatty Liver Disease Pathogenesis.
abstract: Nonalcoholic fatty liver disease (NAFLD), characterized by liver triacylglycerol build-up, has been growing in the global world in concert with the raised prevalence of cardiometabolic disorders, including obesity, diabetes, and hyperlipemia. Redox imbalance has been suggested to be highly relevant to NAFLD pathogenesis. Recent Advances: As a major health problem, NAFLD progresses to the more severe nonalcoholic steatohepatitis (NASH) condition and predisposes susceptible individuals to liver and cardiovascular disease. Although NAFLD represents the predominant cause of chronic liver disorders, the mechanisms of its development and progression remain incompletely understood, even if various scientific groups ascribed them to the occurrence of insulin resistance, dyslipidemia, inflammation, and apoptosis. Nevertheless, oxidative stress (OxS) more and more appears as the most important pathological event during NAFLD development and the hallmark between simple steatosis and NASH manifestation.
  
  
  
  The purpose of this article is to summarize recent developments in the understanding of NAFLD, essentially focusing on OxS as a major pathogenetic mechanism. Various attempts to translate reactive oxygen species (ROS) scavenging by antioxidants into experimental and clinical studies have yielded mostly encouraging results.
  
  
  
  Although augmented concentrations of ROS and faulty antioxidant defense have been associated to NAFLD and related complications, mechanisms of action and proofs of principle should be highlighted to support the causative role of OxS and to translate its concept into the clinic. Antioxid. Redox Signal. 26, 519-541.
authors.affiliation: 1 GI-Nutrition Unit, Research Centre, CHU Ste-Justine, Université de Montréal , Montreal, Quebec, Canada .|2 Department of Nutrition, Université de Montréal , Montreal, Quebec, Canada .
authors.forename: Schohraya
authors.initials: S
authors.lastname: Spahis
authors.affiliation: 1 GI-Nutrition Unit, Research Centre, CHU Ste-Justine, Université de Montréal , Montreal, Quebec, Canada .|3 Department of Biochemistry, Université de Montréal , Montreal, Quebec, Canada .
authors.forename: Edgard
authors.initials: E
authors.lastname: Delvin
authors.affiliation: 4 EPODE International Network , Paris, France .
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Borys
authors.affiliation: 1 GI-Nutrition Unit, Research Centre, CHU Ste-Justine, Université de Montréal , Montreal, Quebec, Canada .|2 Department of Nutrition, Université de Montréal , Montreal, Quebec, Canada .|4 EPODE International Network , Paris, France .
authors.forename: Emile
authors.initials: E
authors.lastname: Levy
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism; D015415:Biomarkers; D059865:Endoplasmic Reticulum Stress; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism; D005786:Gene Expression Regulation; D006505:Hepatitis / Q000209:etiology / Q000378:metabolism; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009154:Mutation; D065626:Non-alcoholic Fatty Liver Disease / Q000209:etiology* / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D008077:Lipoproteins, LDL; D035683:MicroRNAs; D017382:Reactive Oxygen Species; C099252:oxidized low density lipoprotein; D009195:Peroxidase
keywords: antioxidants; cardiometabolic disorders; liver steatosis; mitochondria; reactive oxygen species; treatment