ArticleCellular and molecular life sciences : CMLS2022
The protective effect of selenoprotein M on non-alcoholic fatty liver disease: the role of the AMPKα1-MFN2 pathway and Parkin mitophagy.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 71 citations in OpenAlex.
- Pharmacological Potential of Selenoproteins in the Regulation of Oxidative Stress in Liver Diseases.Pharmaceutics · 2026Review
- Redox-Metabolic Crosstalk in Pediatric MASLD: Biomarkers, Mechanisms, and the Emerging Role of Selenium.International journal of molecular sciences · 2026Review
- Emerging roles of mitophagy in liver fibrosis: Implications for therapy.Acta pharmacologica Sinica · 2026Review
- Mitophagy in Metabolic Dysfunction-Associated Fatty Liver Disease: Mechanisms, Regulatory Networks, and Therapeutic Perspectives.Inflammation · 2026Review
- Integrative analysis of the mouse cecal microbiome across diet, age, and weight in the diverse BXD population.Microbiome · 2026Article
- Natural Product Treatment for Metabolic Dysfunction-Associated Steatotic Liver Disease: Targeted Mitochondrial Quality Control.Drug design, development and therapy · 2026Review
- Mitochondrial Dysfunction in Cardiac Diseases: Insights into Pathophysiology and Clinical Outcomes.Current cardiology reviews · 2026Review
- Selenium and selenoproteins in age-related metabolic diseases: mechanistic insights and translational perspectives.Frontiers in nutrition · 2026Review
- Mechanistic Insights Into the Role of Selenoprotein M in Nickel-Induced Lung Fibrosis.Biological trace element research · 2025Article
- Cell-specific roles of autophagy in liver fibrosis: implications for targeted pharmacotherapy.Annals of medicine · 2025Review
- Selenoprotein M Protects Intestinal Health in Nickel-Exposed Mice: Implications for Animal Welfare Under Heavy Metal Stress.Veterinary sciences · 2025Article
- Review
- Review
- Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity.Journal of advanced research · 2025Article
- Mitochondrial alterations and signatures in hepatocellular carcinoma.Cancer metastasis reviews · 2025Review
- MRPL44 regulates lipid metabolism in metabolic dysfunction-associated steatotic liver disease through BNIP3-mediated mitophagy.Frontiers in nutrition · 2025Article
- Alleviation of Lipid Disorder and Liver Damage in High-Fat Diet-Induced Obese Mice by Selenium-EnrichedNutrients · 2024Article
- Targeting cell death in NAFLD: mechanisms and targeted therapies.Cell death discovery · 2024Review
- Regulatory Role and Cytoprotective Effects of Exogenous Recombinant SELENOM under Ischemia-like Conditions and Glutamate Excitotoxicity in Cortical Cells In Vitro.Biomedicines · 2024Article
- Gut microbial metabolites in MASLD: Implications of mitochondrial dysfunction in the pathogenesis and treatment.Hepatology communications · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is related to a dysregulation of mitophagy, a process that is not fully understood. Parkin-related mitophagy can sustain mitochondrial homeostasis and hepatocyte viability. Herein, we report that selenoprotein M (SELENOM) plays a central role in maintaining mitophagy in high-fat diet (HFD)-mediated NAFLD. We show that SELENOM was significantly downregulated in the liver of HFD-fed mice. SELENOM deletion aggravated HFD-mediated hepatic steatosis, inflammation, and fibrosis; accompanied by enhanced fatty acid oxidation and oxidative stress in the liver. Molecular analyses show that lipotoxicity was related to increased mitochondrial apoptosis as evidenced by enhanced mitochondrial ROS production, and attenuation of mitochondrial potential in the liver of HFD-fed SELENOM
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.