ArticleCell death discovery2023
Altered muscle niche contributes to myogenic deficit in the D2-mdx model of severe DMD.
Article in Cell death discovery, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 25 citations in OpenAlex.
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- 15-PGDH inhibition promotes muscle repair and strength recovery during GLP-1 receptor agonist-induced weight loss.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Macrophage and fibro-adipogenic progenitor communication in skeletal muscle regeneration: tissue homeostasis and pathogenic remodeling.Journal of leukocyte biology · 2026Review
- Stimulation of EGFR signaling in fibro-adipogenic precursors decreases adipogenesis in Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- A Borophosphate Glass Doped with Cobalt Oxide Improves Skeletal Muscle Structure and Function in Myopathic Mice.Journal of functional biomaterials · 2026Article
- Impact of C4BPA on Muscle progenitor cell differentiation: insights for Duchenne muscular dystrophy treatment.Cell death & disease · 2026Article
- 15-PGDH Inhibition Overcomes Muscle Regenerative Deficit Seen With GLP1-Receptor Agonist-Induced Weight Loss.bioRxiv : the preprint server for biology · 2026Article
- CD146 + interstitial cells contribute to the dystrophic skeletal muscle phenotype in vitro.Scientific reports · 2026Article
- The Evolutionarily Conserved TPM1 Super-Enhancer Drives Skeletal Muscle Regeneration via Mechanotransduction Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage plasticity and metabolic control in muscle repair and disease.Frontiers in immunology · 2026Review
- The Landscape of SPP1Immunology · 2025Review
- Short-term daily deflazacort decreases membrane permeability and increases maximum force inAmerican journal of physiology. Cell physiology · 2025Article
- A combinatorial oligonucleotide therapy to improve dystrophin restoration and dystrophin-deficient muscle health.Molecular therapy. Nucleic acids · 2025Article
- Ablation of UCP-1+ cells impacts FAP dynamics in muscle regeneration.American journal of physiology. Cell physiology · 2025Article
- Comparative Transcriptomic Profiling in Patients Affected by Duchenne and Becker Muscular Dystrophies: A Focus on ECM Genes Dysregulation.International journal of molecular sciences · 2025Article
- Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy.Cell death & disease · 2025Article
- SPP1 macrophages across diseases: A call for reclassification?FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Aptamer-conjugated gold nanoparticles enable oligonucleotide delivery into muscle stem cells to promote regeneration of dystrophic muscles.Nature communications · 2025Article
- Engineering of tissue in microphysiological systems demonstrated by modelling skeletal muscle.Regenerative biomaterials · 2025Review
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Authors and funding
12 authors at 2 institutions in 3 countries.
Funding
Abstract
Lack of dystrophin expression is the underlying genetic basis for Duchenne muscular dystrophy (DMD). However, disease severity varies between patients, based on specific genetic modifiers. D2-mdx is a model for severe DMD that exhibits exacerbated muscle degeneration and failure to regenerate even in the juvenile stage of the disease. We show that poor regeneration of juvenile D2-mdx muscles is associated with an enhanced inflammatory response to muscle damage that fails to resolve efficiently and supports the excessive accumulation of fibroadipogenic progenitors (FAPs), leading to increased fibrosis. Unexpectedly, the extent of damage and degeneration in juvenile D2-mdx muscle is significantly reduced in adults, and is associated with the restoration of the inflammatory and FAP responses to muscle injury. These improvements enhance regenerative myogenesis in the adult D2-mdx muscle, reaching levels comparable to the milder B10-mdx model of DMD. Ex vivo co-culture of healthy satellite cells (SCs) with juvenile D2-mdx FAPs reduces their fusion efficacy. Wild-type juvenile D2 mice also manifest regenerative myogenic deficit and glucocorticoid treatment improves their muscle regeneration. Our findings indicate that aberrant stromal cell responses contribute to poor regenerative myogenesis and greater muscle degeneration in juvenile D2-mdx muscles and reversal of this reduces pathology in adult D2-mdx muscle, identifying these responses as a potential therapeutic target for the treatment of DMD.
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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.