ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018
Galectin-3 and N-acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Effect of high-intensity interval training on muscle remodeling in rheumatoid arthritis compared to prediabetes.Arthritis research & therapy · 2018Trial
- Glycobiology-driven therapeutic targeting of glycan-binding proteins: mechanisms, diseases, and clinical translation.Signal transduction and targeted therapy · 2026Review
- Functional role of Galectin-9 in nucleic acid trafficking and transcription post-electrotransfection.NAR molecular medicine · 2026Article
- N-acetylglucosamine facilitates coordinated flow-like movement of myoblasts, forming a foundation for efficient myogenesis.Skeletal muscle · 2025Article
- Improvement of Spontaneous Locomotor Activity in a Murine Model of Duchenne Muscular Dystrophy by N-Acetylglucosamine Alone and in Combination With Prednisolone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Galectin-3: a novel biomarker of glycogen storage disease type III.Cell death discovery · 2025Article
- Targeting Galectin-3 to modulate inflammation in LAMA2-deficient congenital muscular dystrophy.bioRxiv : the preprint server for biology · 2025Article
- Muscle Proteome Analysis of Facioscapulohumeral Dystrophy Patients Reveals a Metabolic Rewiring Promoting Oxidative/Reductive Stress Contributing to the Loss of Muscle Function.Antioxidants (Basel, Switzerland) · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Myoblast-derived exosomes promote the repair and regeneration of injured skeletal muscle in mice.FEBS open bio · 2022Article
- Ruminant conceptus-maternal interactions: interferon-tau and beyond.Journal of animal science · 2022Review
- Optineurin promotes myogenesis during muscle regeneration in mice by autophagic degradation of GSK3β.PLoS biology · 2022Article
- Relationship between Circulating Galectin-3, Systemic Inflammation, and Protein-Energy Wasting in Chronic Hemodialysis Patients.Nutrients · 2021Article
- Regenerative Effects of Hypoxia Primed Flowable Placental Formulation in Muscle and Dermal Injury.International journal of molecular sciences · 2021Article
- Integrated Glycoproteomics Identifies a Role of N-Glycosylation and Galectin-1 on Myogenesis and Muscle Development.Molecular & cellular proteomics : MCP · 2021Article
- Galectin-3 enhances neutrophil motility and extravasation into the airways during Aspergillus fumigatus infection.PLoS pathogens · 2020Article
- Delayed Galectin-3-Mediated Reprogramming of Microglia After Stroke is Protective.Molecular neurobiology · 2019Article
- The Sweet-Side of Leukocytes: Galectins as Master Regulators of Neutrophil Function.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The muscle membrane, sarcolemma, must be firmly attached to the basal lamina. The failure of proper attachment results in muscle injury, which is the underlying cause of Duchenne muscular dystrophy (DMD), in which mutations in the dystrophin gene disrupts the firm adhesion. In patients with DMD, even moderate contraction causes damage, leading to progressive muscle degeneration. The damaged muscles are repaired through myogenesis. Consequently, myogenesis is highly active in patients with DMD, and the repeated activation of myogenesis leads to the exhaustion of the myogenic stem cells. Therefore, approaches to reducing the risk of the exhaustion are to develop a treatment that strengthens the interaction between the sarcolemma and the basal lamina and increases the efficiency of the myogenesis. Galectin-3 is an oligosaccharide-binding protein and is known to be involved in cell-cell interactions and cell-matrix interactions. Galectin-3 is expressed in myoblasts and skeletal muscle, although its function in muscle remains elusive. In this study, we found evidence that galectin-3 and the monosaccharide N-acetylglucosamine, which increases the synthesis of binding partners (oligosaccharides) of galectin-3, promote myogenesis in vitro. Moreover, in the mdx mouse model of DMD, treatment with N-acetylglucosamine increased muscle-force production. The results suggest that treatment with N-acetylglucosamine might mitigate the burden of DMD.-Rancourt, A., Dufresne, S. S., St-Pierre, G., Lévesque, J.-C., Nakamura, H., Kikuchi, Y., Satoh, M. S., Frenette, J., Sato, S. Galectin-3 and N-acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy.
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