Mitochondrial dysfunction in Nash: causes, consequences and possible means to prevent it

Begriche, Karima; Igoudjil, Anissa; Pessayre, Dominique; Fromenty, Bernard

doi:10.1016/j.mito.2005.10.004

Cited by 753Liver Disease Diagnosis and TreatmentMitochondrial Function and PathologyDrug-Induced Hepatotoxicity and Protection

Mitochondrial dysfunction in Nash: causes, consequences and possible means to prevent it

Begriche, Karima, Igoudjil, Anissa, Pessayre, Dominique, Fromenty, Bernard·2006·Mitochondrion

DOI 10.1016/j.mito.2005.10.004

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Abstract

Calorie-enriched diet and lack of exercise are causing a worldwide surge of obesity, insulin resistance and lipid accretion in liver (i.e. hepatic steatosis), which can lead to steatohepatitis. Steatosis and nonalcoholic steatohepatitis (NASH) can also be induced by drugs such as amiodarone, tamoxifen and some antiretroviral drugs, including stavudine and zidovudine. There is accumulating evidence that mitochondrial dysfunction (more particularly respiratory chain deficiency) plays a key role in the physiopathology of NASH whatever its initial cause. In contrast, the mitochondrial beta-oxidation of fatty acids can be either increased (as in insulin resistance-associated NASH) or decreased (as in drug-induced NASH). However, in both circumstances, generation of reactive oxygen species (ROS) by the damaged respiratory chain can be augmented. ROS generation in an environment enriched in lipids in turn induces lipid peroxidation which releases highly reactive aldehydic derivatives (e.g. malondialdehyde) that have diverse detrimental effects on hepatocytes and other hepatic cells. In hepatocytes, ROS, reactive nitrogen species and lipid peroxidation products further impair the respiratory chain, either directly or indirectly through oxidative damage to the mitochondrial genome. This consequently leads to the generation of more ROS and a vicious cycle occurs. Mitochondrial dysfunction can also lead to apoptosis or necrosis depending on the energy status of the cell. ROS and lipid peroxidation products also increase the generation of several cytokines (TNF-alpha, TGF-beta, Fas ligand) playing a key role in cell death, inflammation and fibrosis. Recent investigations have shown that some genetic polymorphisms can significantly increase the risk of steatohepatitis and that several drugs can prevent or even reverse NASH. Interestingly, most of these drugs could exert their beneficial effects by improving directly or indirectly mitochondrial function in liver. Finding a drug, which could fully prevent oxidative stress and mitochondrial dysfunction in NASH is a major challenge for the next decade.

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An increase in Cytochrome C expression implies activation of its function as a single electron carrier in the electron transport chain, catalyzing the reduction of oxygen to water and leading to more ATP.
“An increase in expression of Cytochrome C implies activation of its function as a single electron carrier in the electron transport chain catalyzing the reduction of oxygen molecule to water, thus leading to more ATP [34].”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [34]
In patients with NASH, an increase in ROS is associated with impaired mitochondrial electron transport chain (ETC) and loss in ΔΨm.
“In patients with NASH, an increase in the ROS is associated with impaired mitochondrial electron transport chain (ETC) and loss in the ΔΨm [34].”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [34]
An increase in ROS damages mitochondrial DNA.
“Also, increase in the ROS is shown to damage mitochondrial DNA [43].”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [43]
Mitochondrial DNA is extremely sensitive to oxidative/nitrative damage due to its location closer to the inner mitochondrial membrane, relatively low amounts of histone, anti-oxidant enzymes and mtGSH, and low levels of polyamines and DNA repair enzymes.
“Indeed, mitochondrial DNA is extremely sensitive to oxidative/nitrative damage due to (A) its location closer to the inner mitochondrial membrane; (B) the relatively low amount of histone, anti-oxidant enzymes, and mtGSH, and (C) the low levels of polyamines and DNA repair enzymes [78], [79].”
From Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications (2014) · cites this paper as [79]

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Self-citation
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Authors: Begriche, K., Igoudjil, A., Pessayre, D., & Fromenty, B.
Affiliations: Inserm (FR)
Corresponding author: Fromenty, Bernard
ORCID: Begriche, Karima
Fromenty, Bernard
Venue: Mitochondrion
Publisher: Elsevier BV
Published: 2006-02
Volume: 6
Issue: 1
Pages: 1-28
ISSN: 1567-7249 (ISSN-L)
DOI: 10.1016/j.mito.2005.10.004
OpenAlex: W1978045299
Cited by: 753
References: 348
Citations by year: 2026: 24 · 2025: 28 · 2024: 33 · 2023: 27 · 2022: 55 · 2021: 47 · 2020: 43 · 2019: 48 · 2018: 43 · 2017: 32 · 2016: 39 · 2015: 39 · 2014: 38 · 2013: 39 · 2012: 35
FWCI: 4.46
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Mitochondrion (publishedVersion)
PubMed (publishedVersion)
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: mitochondrial dysfunction, nonalcoholic steatohepatitis, hepatic steatosis, respiratory chain deficiency, reactive oxygen species, lipid peroxidation, malondialdehyde, mitochondrial DNA damage, insulin resistance, drug-induced liver injury, fatty acid beta-oxidation, apoptosis, cytokines, liver fibrosis, genetic polymorphism, oxidative stress
MeSH terms: Animals, Drug Therapy, Fatty Liver, Hepatitis, Humans, Mitochondria, Liver, Mitochondrial Diseases, Lipid Metabolism

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Mitochondrial dysfunction in Nash: causes, consequences and possible means to prevent it

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