ArticleInternational journal of molecular sciences2021
The Alterations of Mitochondrial Function during NAFLD Progression-An Independent Effect of Mitochondrial ROS Production.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- Targeting Mitochondria in MASLD: Comparative Evaluation of MitoQ and SS-31 (Elamipretide) in Aged Female Mice under Nutritional Stress.Physiological research · 2026Article
- Hypoxia in MASLD: a spatial determinant of the pathogenesis.Trends in molecular medicine · 2026Review
- Mitochondrial Dysfunction in Metabolic-Syndrome-Related MASLD/MASH: Metabolic Mechanisms and Therapeutic Perspectives.Metabolites · 2026Review
- Diverse Forms of Autophagy and Their Roles in Liver Disease and Aging: A Comprehensive Review.Proteomes · 2026Review
- NAMPT improves high-fat diet-induced nonalcoholic fatty liver disease (NAFLD) via the SIRT1-C/EBPβ-STEAP4-NRF2 axis.Journal of molecular cell biology · 2026Article
- Biomarkers for early identification of metabolic dysfunction-associated steatotic liver disease (MASLD): a narrative review.Archives of medical science : AMS · 2026Article
- Oxidative Stress in Liver Metabolic Dysfunction and Diseases, with a Focus on Hepatogenic Diabetes: Effect of Alcohol Consumption.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Zebrafish model of palmitic acid induced MAFLD recapitulates pathways conserved in mice and humans.Scientific reports · 2025Article
- The Naturally Bioactive Vicine Extracted from Faba Beans Is Responsible for the Transformation of Grass Carp (Antioxidants (Basel, Switzerland) · 2025Article
- Management of metabolic dysfunction-associated steatotic liver disease (MASLD)-An expert consensus statement from Indian diabetologists' perspective.Diabetes, obesity & metabolism · 2025Review
- Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Influence of Lipid Class Used for Omega-3 Fatty Acid Supplementation on Liver Fat Accumulation in MASLD.Physiological research · 2024Review
- The Interplay between Endogenous and Foodborne Pro-Oxidants and Antioxidants in Shaping Redox Homeostasis.International journal of molecular sciences · 2024Review
- Si-Wu-Tang alleviates metabolic dysfunction-associated fatty liver disease by inhibiting ACSL4-mediated arachidonic acid metabolism and ferroptosis in MCD diet-fed mice.Chinese medicine · 2024Article
- Updated mechanisms of MASLD pathogenesis.Lipids in health and disease · 2024Review
- ACACA reduces lipid accumulation through dual regulation of lipid metabolism and mitochondrial function via AMPK- PPARα- CPT1A axis.Journal of translational medicine · 2024Article
- Dietary intervention reverses molecular markers of hepatocellular senescence in the GAN diet-induced obese and biopsy-confirmed mouse model of NASH.BMC gastroenterology · 2024Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
The progression of non-alcoholic fatty liver (NAFL) into non-alcoholic steatohepatitis implicates multiple mechanisms, chief of which is mitochondrial dysfunction. However, the sequence of events underlying mitochondrial failure are still poorly clarified. In this work, male C57BL/6J mice were fed with a high-fat plus high-sucrose diet for 16, 20, 22, and 24 weeks to induce NAFL. Up to the 20th week, an early mitochondrial remodeling with increased OXPHOS subunits levels and higher mitochondrial respiration occurred. Interestingly, a progressive loss of mitochondrial respiration along "Western diet" feeding was identified, accompanied by higher susceptibility to mitochondrial permeability transition pore opening. Importantly, our findings prove that mitochondrial alterations and subsequent impairment are independent of an excessive mitochondrial reactive oxygen species (ROS) generation, which was found to be progressively diminished along with disease progression. Instead, increased peroxisomal abundance and peroxisomal fatty acid oxidation-related pathway suggest that peroxisomes may contribute to hepatic ROS generation and oxidative damage, which may accelerate hepatic injury and disease progression. We show here for the first time the sequential events of mitochondrial alterations involved in non-alcoholic fatty liver disease (NAFLD) progression and demonstrate that mitochondrial ROS are not one of the first hits that cause NAFLD progression.
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