Mitochondrial Dysfunction and Signaling in Chronic Liver Diseases.
By A. Mansouri, Charles-Henry Gattolliat, T. Asselah. Gastroenterology, 2018
687 citations recorded by the source corpus.
Mitochondria regulate hepatic lipid metabolism and oxidative stress. Ultrastructural mitochondrial lesions, altered mitochondrial dynamics, decreased activity of respiratory chain complexes, and impaired ability to synthesize adenosine triphosphate are observed in liver tissues from patients with alcohol-associated and non-associated liver diseases. Increased lipogenesis with decreased fatty acid β-oxidation leads to the accumulation of triglycerides in hepatocytes, which, combined with increased levels of reactive oxygen species, contributes to insulin resistance in patients with steatohepatitis. Moreover, mitochondrial reactive oxygen species mediate metabolic pathway signaling; alterations in these pathways affect development and progression of chronic liver diseases. Mitochondrial stress and lesions promote cell death, liver fibrogenesis, inflammation, and the innate immune responses to viral infections. We review the involvement of mitochondrial processes in development of chronic liver diseases, such as nonalcoholic fatty, alcohol-associated, and drug-associated liver diseases, as well as hepatitis B and C, and discuss how they might be targeted therapeutically.
Subfields: Epidemiology, Hepatology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/432ecad8cce31419f02c85fd1eaf7562428d426e
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Citations in the corpus
- PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “There is evidence to suggest that mitochondrial dysfunction and decreased fatty acid oxidation play a central role in the pathogenesis of NAFLD [202].”
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, positive): “400,405 An inhibition in mitochondrial fusion, especially caused by the down-regulation of Mfn, is closely related to liver diseases due to an impairment in fatty acid oxidation, the TCA cycle, and glycolysis.”