ArticleJournal of advanced research2026
Loss of hepatic ME1 ameliorates MASLD by Suppressing peroxisomal β-Oxidation and Activating Lipophagy/Lipolysis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Peroxisomes in Liver Diseases: From Metabolite Quality Control to Inter-Organelle and Inter-Organ Signaling.Biomolecules · 2026Review
- Analysis of the immunomodulatory effects of Honeysuckle leaf polysaccharides on cherry valley ducks based on transcriptomic techniques.Poultry science · 2026Article
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
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Authors and funding
13 authors.
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Abstract
introductionMetabolic dysfunction-associated steatotic liver disease (MASLD) represents an increasing global health problem in association with obesity and insulin resistance without approved pharmacotherapy. Previous studies revealed malic enzyme 1 (ME1) as a susceptibility gene for metabolic disorders in humans. However, the role and mechanisms of ME1 in regulating hepatic lipid metabolism remain largely unclear.
objectivesThis study aimed to investigate the roles, mechanisms, and therapeutic potential of ME1 in regulating MASLD.
methodsHepatic expression of ME1 gene and protein were characterized in MASLD patients and three MASLD mouse models. Using a hepatocyte-specific Me1 knockout model, we assessed the effects of the gene on diet-induced or age-dependent MASLD. Oleic and palmitic acids were used to mimic hepatic lipid accumulation in vitro. Molecular mechanisms underlying ME1 function were investigated through RNA sequencing, biochemical analyses, and pharmacological intervention.
resultsME1 demonstrates a positive correlation with MASLD progression in both mouse models and human patients. Hepatocyte-specific deletion of Me1 gene reduced body weight, attenuated insulin resistance, and improved hepatic steatosis after 16 weeks of high-fat diet (HFD) feeding. Besides, the detrimental effects of Me1 on fatty liver and associated pathologies are observed in aged knockout mice. Conversely, overexpressing ME1 exacerbated MASLD in vitro and in vivo. Transcriptome analyses uncovered that in response to HFD, acyl-CoA oxidase 1 (Acox1)-mediated peroxisomal fatty acid β-oxidation was remarkably suppressed in Me1-deficient livers, thereby disrupting the downstream production of acetyl-CoA and H
conclusionsOur study provides the first demonstration that ME1 regulates ACOX1-mediated peroxisomal β-oxidation and subsequent lipophagy/lipolysis, revealing its pivotal lipid-regulatory role in MASLD. These findings underscore ME1 as a promising target for treating MASLD and associated liver pathologies.
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