Mitochondria in non-alcoholic fatty liver disease

• Published in: The international journal of biochemistry & cell biology Vol. 95; pp. 93 - 99
• Main Authors: Simões, Inês C.M., Fontes, Adriana, Pinton, Paolo, Zischka, Hans, Wieckowski, Mariusz R.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.02.2018
• Subjects: Mitochondria; NAFLD; NASH; ROS; Steatosis; FFA; JNK; HFD; ALT; OXPHOS; MDA; Gpx; apoB; MPT; NF-κB; Mitochondria; RNS; UPR; VLDL; iNOS; PPAR-α; IL; Δym; IR; ER; TCA; miR; ROS; AMPK; TFAM; CPT-1; NADPH; NO; NAFLD; mtDNA; NRF-2; UCP2; mtFAO; TLR; GSH; 8-OHdG; mtGSH; AST; PGC-1α; NASH; SOD2; Steatosis; TG; TNF-α; ETC; FAO; DNA; ATP; HNE
• ISSN: 1357-2725; 1878-5875; 1878-5875
• DOI: 10.1016/j.biocel.2017.12.019

•Increased mitochondrial activity protects hepatocytes from the deleterious effects of FFAs deposition.•Hepatic mitochondria are structurally and molecularly altered in NAFLD.•Mitochondrial dysfunction in animal models of NAFLD is characterized by alterations in the abundance and activity of OXPHOS proteins.•Decline in mitochondrial function provokes metabolic disturbances and may potentially contribute to NAFLD progression.•Increased mitochondrial cholesterol accumulation is related with the progression of steatosis to steatohepatitis. 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.