Mitochondria in non-alcoholic fatty liver disease
Open accessAbstract
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.
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Disruption in complexes I and III increases formation of ROS, diminishes tGSH, and depletes ATP generation.
“Disruption in the complexes I and III has shown to increase formation of ROS, diminish tGSH, and deplete ATP generation [42].”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [42]
Section 2.2.2 identifies complexes I and III as major sites of superoxide production and reports diminished GSH-related antioxidant activity in NAFLD. Section 2.1.2 reports reduced ATP synthesis alongside ETC alterations. The paper does not establish that disruption of complexes I and III specifically causes all three effects, or that total glutathione (tGSH) is depleted. (LLM, conf=0.87)
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Sunny, N. E., Parks, E. J., Browning, J. D., & Burgess, S. C. (2011) · Cell Metabolism · doi:10.1016/j.cmet.2011.11.004 · Cited by 672 · see citing works
Mitochondrial adaptation in steatotic mice
Einer, C., Hohenester, S., Wimmer, R., Wottke, L., Artmann, R., Schulz, S., Gosmann, C., Simmons, A., Leitzinger, C., Eberhagen, C., et al. (2018) · Mitochondrion · doi:10.1016/j.mito.2017.08.015 · Cited by 72 · see citing works
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Inflammatory signaling in NASH driven by hepatocyte mitochondrial dysfunctions
Myint, M., Oppedisano, F., De Giorgi, V., Kim, B.-M., Marincola, F. M., Alter, H. J., & Nesci, S. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04627-0 · Cited by 61 · see citing works
Huang, L., Zeng, X., Li, B., Wang, C., Zhou, M., Lang, H., Yi, L., & Mi, M. (2021) · Nutrition & Metabolism · doi:10.1186/s12986-021-00612-w · Cited by 23 · see citing works
Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells
Dhami-Shah, H., Vaidya, R., Talwadekar, M., Shaw, E., Udipi, S., Kolthur-Seetharam, U., & Vaidya, A. D. B. (2021) · Journal of Ayurveda and Integrative Medicine · doi:10.1016/j.jaim.2021.04.007 · Cited by 15 · see citing works
“Disruption in the complexes I and III has shown to increase formation of ROS, diminish tGSH, and deplete ATP generation [42].”
Background
- Authors
- Simões, I. C. M., Fontes, A., Pinton, P., Zischka, H., & Wieckowski, M. R.
- Affiliations
- Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
- Helmholtz Munich (DE)
- University of Ferrara (IT)
- Corresponding author
- Wieckowski, Mariusz R.
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 95
- Pages
- 93-99
- ISSN
- 1357-2725 (ISSN-L)
- OpenAlex
- W2777277563
- Cited by
- 234
- References
- 2
- Citations by year
- 2026: 5 · 2025: 16 · 2024: 24 · 2023: 32 · 2022: 37 · 2021: 50 · 2020: 25 · 2019: 29 · 2018: 15 · 2012: 1
- FWCI
- 2.50
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion, cc-by-nc-nd)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion, other-oa)
- Site cant be reached (submittedVersion, cc-by-nc-nd)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion, cc-by-nc-nd)
- Funders
- FOIE GRAS
- mtFOIE GRAS
- European Union’s Horizon 2020 Research and Innovation programme (722619, 734719)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- non-alcoholic fatty liver disease, mitochondria, mitochondrial dysfunction, reactive oxygen species, oxidative stress, steatosis, steatohepatitis, liver inflammation, disease progression
- MeSH terms
- Animals, Humans, Mitochondria, Liver, Oxidation-Reduction, Severity of Illness Index, Reactive Oxygen Species, Oxidative Stress, Disease Progression, End Stage Liver Disease, Non-alcoholic Fatty Liver Disease
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