ArticleFrontiers in endocrinology2023
Exercise intervention improves mitochondrial quality in non-alcoholic fatty liver disease zebrafish.
Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Metabolic dysfunction-associated steatotic liver disease: pathogenic mechanisms and exercise-induced molecular adaptations.Lipids in health and disease · 2026Review
- A Framework for Selecting Zebrafish Models of Metabolic Diseases: Modeling Strategies, Phenotypic Validation, Mechanistic Investigation, and Efficacy Evaluation.Biomedicines · 2026Review
- Exercise and dietary interventions in the regulation of hepatic mitophagy and liver recovery (Review).Biomedical reports · 2026Review
- Restoring Mitochondrial Homeostasis: Therapeutic Strategies for Metabolic Dysfunction-Associated Fatty Liver Disease.International journal of molecular sciences · 2026Review
- Exercise as a Molecular Therapeutic Tool in MASLD: From Signaling Pathways to Clinical Translation-A Narrative Review.Biomedicines · 2026Review
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- Review
- Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025Review
- Exercise training and Silymarin consumption can ameliorate mitophagy signaling flux in hepatocytes of rats with dexamethasone-induced non-alcoholic fatty liver disease.Scientific reports · 2025Article
- Protective effect of exercise on metabolic dysfunction‑associated fatty liver disease: Potential epigenetic mechanisms (Review).International journal of molecular medicine · 2025Review
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Roles of olive oil and physical exercise in non-alcoholic fatty liver disease after ultrasound-based evaluation.World journal of hepatology · 2025Article
- Understanding the Role of Exercise and Probiotic Interventions on Non-Alcoholic Fatty Liver Disease Alleviation in Zebrafish: Dialogue Between the Gut and Liver.International journal of molecular sciences · 2025Article
- Potential Synergistic Effects of Caffeine and Naringin on Mitochondrial Biogenesis and Hepatic Steatosis in Adult Male Rats With NAFLD Induced by a High-Fat Diet.BioMed research international · 2025Article
- Article
- Exercise Alleviates Cardiovascular Diseases by Improving Mitochondrial Homeostasis.Journal of the American Heart Association · 2024Review
- Altered Mitochondrial Function in MASLD: Key Features and Promising Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2024Review
- Liver Cell Mitophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis.Antioxidants (Basel, Switzerland) · 2024Review
- The role of mitophagy in metabolic diseases and its exercise intervention.Frontiers in physiology · 2024Review
- Mitophagy in fibrotic diseases: molecular mechanisms and therapeutic applications.Frontiers in physiology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Recent reports indicate that mitochondrial quality decreases during non-alcoholic fatty liver disease (NAFLD) progression, and targeting the mitochondria may be a possible treatment for NAFLD. Exercise can effectively slow NAFLD progression or treat NAFLD. However, the effect of exercise on mitochondrial quality in NAFLD has not yet been established. Methods: In the present study, we fed zebrafish a high-fat diet to model NAFLD, and subjected the zebrafish to swimming exercise. Results: After 12 weeks, swimming exercise significantly reduced high-fat diet-induced liver injury, and reduced inflammation and fibrosis markers. Swimming exercise improved mitochondrial morphology and dynamics, inducing upregulation of optic atrophy 1(OPA1), dynamin related protein 1 (DRP1), and mitofusin 2 (MFN2) protein expression. Swimming exercise also activated mitochondrial biogenesis via the sirtuin 1 (SIRT1)/ AMP-activated protein kinase (AMPK)/ PPARgamma coactivator 1 alpha (PGC1α) pathway, and improved the mRNA expression of genes related to mitochondrial fatty acid oxidation and oxidative phosphorylation. Furthermore, we find that mitophagy was suppressed in NAFLD zebrafish liver with the decreased numbers of mitophagosomes, the inhibition of PTEN-induced kinase 1 (PINK1) - parkin RBR E3 ubiquitin protein ligase (PARKIN) pathway and upregulation of sequestosome 1 (P62) expression. Notably, swimming exercise partially recovered number of mitophagosomes, which was associated with upregulated PARKIN expression and decreased p62 expression. Discussion: These results demonstrate that swimming exercise could alleviate the effects of NAFLD on the mitochondria, suggesting that exercise may be beneficial for treating NAFLD.
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