ArticleRedox biology2019
SELENON (SEPN1) protects skeletal muscle from saturated fatty acid-induced ER stress and insulin resistance.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 59 citations in OpenAlex.
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- Article
- Selenoprotein N and SEPN1-Related Myopathies: Mechanisms, Models, and Therapeutic Perspectives.Biomolecules · 2026Review
- A Novel LAMA2 Mutation (c.7412G>A) Was Found in a Chinese Patient With Congenital Muscular Dystrophy.Journal of cellular and molecular medicine · 2025Article
- Selenium and Skeletal Muscle Health in Sports Nutrition.Nutrients · 2025Review
- Zebrafish and cellular models of SELENON-Congenital myopathy exhibit novel embryonic and metabolic phenotypes.Skeletal muscle · 2025Article
- SELENON-related myopathy as a cause of acute respiratory failure in middle age: a case report.Journal of medical case reports · 2025Article
- Selenium and Selenoproteins: Mechanisms, Health Functions, and Emerging Applications.Molecules (Basel, Switzerland) · 2025Review
- Proteomics Analysis of the Protective Effect of Polydeoxyribonucleotide Extracted from Sea Cucumber (Marine drugs · 2024Article
- SEPN1-related myopathy depends on the oxidoreductase ERO1A and is druggable with the chemical chaperone TUDCA.Cell reports. Medicine · 2024Article
- Clozapine suppresses NADPH oxidase activation, counteracts cytosolic HRedox biology · 2023Article
- CaInternational journal of molecular sciences · 2023Article
- Loss-of-rescue of Ryr1Scientific reports · 2022Article
- Selenium status and type 2 diabetes risk.Archives of biochemistry and biophysics · 2022Review
- Defining and identifying satellite cell-opathies within muscular dystrophies and myopathies.Experimental cell research · 2022Article
- Beyond antioxidants: Selenium and skeletal muscle mitochondria.Frontiers in veterinary science · 2022Review
- NovelFrontiers in genetics · 2022Article
- Role of mitochondria-associated endoplasmic reticulum membranes in insulin sensitivity, energy metabolism, and contraction of skeletal muscle.Frontiers in molecular biosciences · 2022Review
- Review
- Dietary Marginal and Excess Selenium Increased Triglycerides Deposition, Induced Endoplasmic Reticulum Stress and Differentially Influenced Selenoproteins Expression in the Anterior and Middle Intestines of Yellow CatfishAntioxidants (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenoprotein N (SELENON) is an endoplasmic reticulum (ER) protein whose loss of function leads to a congenital myopathy associated with insulin resistance (SEPN1-related myopathy). The exact cause of the insulin resistance in patients with SELENON loss of function is not known. Skeletal muscle is the main contributor to insulin-mediated glucose uptake, and a defect in this muscle-related mechanism triggers insulin resistance and glucose intolerance. We have studied the chain of events that connect the loss of SELENON with defects in insulin-mediated glucose uptake in muscle cells and the effects of this on muscle performance. Here, we show that saturated fatty acids are more lipotoxic in SELENON-devoid cells, and blunt the insulin-mediated glucose uptake of SELENON-devoid myotubes by increasing ER stress and mounting a maladaptive ER stress response. Furthermore, the hind limb skeletal muscles of SELENON KO mice fed a high-fat diet mirrors the features of saturated fatty acid-treated myotubes, and show signs of myopathy with a compromised force production. These findings suggest that the absence of SELENON together with a high-fat dietary regimen increases susceptibility to insulin resistance by triggering a chronic ER stress in skeletal muscle and muscle weakness. Importantly, our findings suggest that environmental cues eliciting ER stress in skeletal muscle (such as a high-fat diet) affect the pathological phenotype of SEPN1-related myopathy and can therefore contribute to the assessment of prognosis beyond simple genotype-phenotype correlations.
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