Format

Send to

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

Mitochondria in non-alcoholic fatty liver disease.

Author information

1
Department of Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Pasteur 3 Str., 02-093 Warsaw, Poland.
2
Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, D-85764, Neuherberg, Germany.
3
Department of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
4
Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, D-85764, Neuherberg, Germany; Institute of Toxicology and Environmental Hygiene, Technical University Munich, Biedersteiner Straße 29, D-80802 Munich, Germany.
5
Department of Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Pasteur 3 Str., 02-093 Warsaw, Poland. Electronic address: m.wieckowski@nencki.gov.pl.

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

PMID:
29288054
DOI:
10.1016/j.biocel.2017.12.019
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center