ArticleDiabetologia2021
Non-alcoholic fatty liver disease in mice with hepatocyte-specific deletion of mitochondrial fission factor.
Article in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 51 citations in OpenAlex.
- Bariatric surgery may alleviate MASLD by restoring mitochondria-lipid droplet structural and functional integrity through suppression of the Mitochondrial Fission Factor-Perilipin 5 axis.Molecular biomedicine · 2026Article
- Mitochondrial Distress Signals at the Heart-Liver Interface: Molecular Links Between MASLD and Heart Failure.International journal of molecular sciences · 2026Review
- Mitochondrial Dysfunction in Metabolic-Syndrome-Related MASLD/MASH: Metabolic Mechanisms and Therapeutic Perspectives.Metabolites · 2026Review
- Restoring Mitochondrial Homeostasis: Therapeutic Strategies for Metabolic Dysfunction-Associated Fatty Liver Disease.International journal of molecular sciences · 2026Review
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Chondroitin Sulfate as a Lysosomal Enhancer Attenuates Lipid-Driven Inflammation via Lipophagy and Mitophagy.Marine drugs · 2025Article
- Melanocortin 3 receptor regulates hepatic autophagy and systemic adiposity.Nature communications · 2025Article
- The Role of Mitochondrial Quality Control in Liver Diseases: Dawn of a Therapeutic Era.International journal of biological sciences · 2025Review
- Article
- MICOS Complex Loss Governs Age-Associated Murine Mitochondrial Architecture and Metabolism in the Liver, While Sam50 Dictates Diet Changes.bioRxiv : the preprint server for biology · 2024Article
- Signaling through the nicotinic acetylcholine receptor in the liver protects against the development of metabolic dysfunction-associated steatohepatitis.PLoS biology · 2024Article
- Vitamin D ameliorates age-induced nonalcoholic fatty liver disease by increasing the mitochondrial contact site and cristae organizing system (MICOS) 60 level.Experimental & molecular medicine · 2024Article
- Targeting mitochondrial homeostasis in the treatment of non-alcoholic fatty liver disease: a review.Frontiers in pharmacology · 2024Review
- Mitochondrial Dysfunction in Metabolic Dysfunction Fatty Liver Disease (MAFLD).International journal of molecular sciences · 2023Review
- mTORC2-NDRG1-CDC42 axis couples fasting to mitochondrial fission.Nature cell biology · 2023Article
- Early-onset caloric restriction alleviates ageing-associated steatohepatitis in male mice via restoring mitochondrial homeostasis.Biogerontology · 2023Article
- Hepatic Mitochondria-Gut Microbiota Interactions in Metabolism-Associated Fatty Liver Disease.Metabolites · 2023Review
- Exercise intervention improves mitochondrial quality in non-alcoholic fatty liver disease zebrafish.Frontiers in endocrinology · 2023Article
- Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisMitochondria are highly dynamic organelles continuously undergoing fission and fusion, referred to as mitochondrial dynamics, to adapt to nutritional demands. Evidence suggests that impaired mitochondrial dynamics leads to metabolic abnormalities such as non-alcoholic steatohepatitis (NASH) phenotypes. However, how mitochondrial dynamics are involved in the development of NASH is poorly understood. This study aimed to elucidate the role of mitochondrial fission factor (MFF) in the development of NASH.
methodsWe created mice with hepatocyte-specific deletion of MFF (MffLiKO). MffLiKO mice fed normal chow diet (NCD) or high-fat diet (HFD) were evaluated for metabolic variables and their livers were examined by histological analysis. To elucidate the mechanism of development of NASH, we examined the expression of genes related to endoplasmic reticulum (ER) stress and lipid metabolism, and the secretion of triacylglycerol (TG) using the liver and primary hepatocytes isolated from MffLiKO and control mice.
resultsMffLiKO mice showed aberrant mitochondrial morphologies with no obvious NASH phenotypes during NCD, while they developed full-blown NASH phenotypes in response to HFD. Expression of genes related to ER stress was markedly upregulated in the liver from MffLiKO mice. In addition, expression of genes related to hepatic TG secretion was downregulated, with reduced hepatic TG secretion in MffLiKO mice in vivo and in primary cultures of MFF-deficient hepatocytes in vitro. Furthermore, thapsigargin-induced ER stress suppressed TG secretion in primary hepatocytes isolated from control mice. CONCLUSIONS/
interpretationWe demonstrated that ablation of MFF in liver provoked ER stress and reduced hepatic TG secretion in vivo and in vitro. Moreover, MffLiKO mice were more susceptible to HFD-induced NASH phenotype than control mice, partly because of ER stress-induced apoptosis of hepatocytes and suppression of TG secretion from hepatocytes. This study provides evidence for the role of mitochondrial fission in the development of NASH.
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