ArticleNature communications2023
Clearance of defective muscle stem cells by senolytics restores myogenesis in myotonic dystrophy type 1.
Article in Nature communications, 2023. 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, 32 citations in OpenAlex.
- MAPK-driven MYC/p21 axis controls senescence bypass and BCL-XL dependence in vincristine-resistant rhabdomyosarcoma.iScience · 2026Article
- MBNL depletion drives stem cell fusion and immature myonuclear states in myotonic dystrophy type 1.Nature communications · 2026Article
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- The role and potential therapeutic intervention of cellular senescence in intervertebral disc degeneration.Genes & diseases · 2026Review
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Characterization of p16-positive stromal cells in age-related cardiac disorders.Journal of biochemistry · 2026Article
- Commitment to Myogenic Differentiation Significantly Aggravates the RNA Phenotype in Myotonic Dystrophy Type 1.Neuropathology and applied neurobiology · 2026Article
- The Immunogenicity of Human Senescent Cells Is Dependent on the Senescence Inducer and Cell Type.Aging cell · 2026Article
- Convergent innate immune and regulated cell-death pathways in selected myopathies.Frontiers in immunology · 2026Review
- Identification of enzymatically modified isoquercitrin as a therapeutic lead for myotonic dystrophy type 1.NAR molecular medicine · 2026Article
- Lineage relationships in muscle stem cells: linking functional fate to molecular state.Frontiers in cell and developmental biology · 2026Review
- A 12-Week Strength Training Improves Mitochondrial Respiration, HActa physiologica (Oxford, England) · 2025Article
- Loss of cell-autonomously secreted laminin-α2 drives muscle stem cell dysfunction in LAMA2-related muscular dystrophy.Nature communications · 2025Article
- Bioactive lipid mediator class switching regulates myogenic cell progression and muscle regeneration.Nature communications · 2025Article
- AAV capsids target muscle-resident cells with different efficiencies-A comparative study between AAV8, AAVMYO, and AAVMYO2.Molecular therapy. Methods & clinical development · 2025Article
- Muscle stem cells in Duchenne muscular dystrophy exhibit molecular impairments and altered cell fate trajectories impacting regenerative capacity.Cell death & disease · 2025Article
- Multisystem Symptoms in Myotonic Dystrophy Type 1: A Management and Therapeutic Perspective.International journal of molecular sciences · 2025Review
- The influence of age on cellular senescence in injured versus healthy muscle and its implications on rotator cuff injuries.Journal of shoulder and elbow surgery · 2025Article
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Myotonic dystrophies: an update on clinical features, molecular mechanisms, management, and gene therapy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
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22 authors at 4 institutions in 1 country.
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Abstract
Muscle stem cells, the engine of muscle repair, are affected in myotonic dystrophy type 1 (DM1); however, the underlying molecular mechanism and the impact on the disease severity are still elusive. Here, we show using patients' samples that muscle stem cells/myoblasts exhibit signs of cellular senescence in vitro and in situ. Single cell RNAseq uncovers a subset of senescent myoblasts expressing high levels of genes related to the senescence-associated secretory phenotype (SASP). We show that the levels of interleukin-6, a prominent SASP cytokine, in the serum of DM1 patients correlate with muscle weakness and functional capacity limitations. Drug screening revealed that the senolytic BCL-XL inhibitor (A1155463) can specifically remove senescent DM1 myoblasts by inducing their apoptosis. Clearance of senescent cells reduced the expression of SASP, which rescued the proliferation and differentiation capacity of DM1 myoblasts in vitro and enhanced their engraftment following transplantation in vivo. Altogether, this study identifies the pathogenic mechanism associated with muscle stem cell defects in DM1 and opens a therapeutic avenue that targets these defective cells to restore myogenesis.
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