ArticleCell death & disease2023
Decoding the transcriptome of Duchenne muscular dystrophy to the single nuclei level reveals clinical-genetic correlations.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Evaluation of a serum protein signature as monitoring biomarker for Duchenne muscular dystrophy in a long-term clinical trial with corticosteroids.Skeletal muscle · 2026Trial
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Mutation-agnostic base editing of the progerin farnesylation site rescues Hutchinson-Gilford progeria syndrome phenotypes in neuromuscular organoids.Nature communications · 2026Article
- Article
- Network medicine and single-cell mapping identify a collagen-rich, fibrosis-associated hub module in Duchenne muscular dystrophy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Unraveling the spatial landscape of dystrophinopathies: a transcriptomic approach to Becker and Duchenne muscular dystrophies.The Journal of pathology · 2026Article
- MDBiomarkers: A queryable biomarkers database integrating multiple serum and tissue datasets for Duchenne muscular dystrophy.Journal of neuromuscular diseases · 2026Article
- Single nuclei/cell transcriptomics reveal DMD driven cell dynamics and mechanisms of fibroblast inflammatory tissue priming in human dystrophic muscle.Research square · 2026Article
- Impact of C4BPA on Muscle progenitor cell differentiation: insights for Duchenne muscular dystrophy treatment.Cell death & disease · 2026Article
- Investigating the role of EGFR signalling in muscle dystrophies: implications for Duchenne muscular dystrophy.Cell death & disease · 2026Article
- Evaluation of a serum protein signature as monitoring biomarker for Duchenne Muscular Dystrophy in a long-term clinical trial with corticosteroids.medRxiv : the preprint server for health sciences · 2026Article
- Transcriptomics-based analysis of muscle injury mechanism mediated by inflammatory imbalance in the Duchenne muscular dystrophy muscle microenvironment.Frontiers in neurology · 2026Article
- Circulating protein biomarkers identified in two independent clinical trial cohorts of glucocorticoid-naive Duchenne muscular dystrophy patients.Scientific reports · 2025Article
- Dystrophin Restorative and Compensatory Gene Addition Therapies for Duchenne Muscular Dystrophy: Could CRISPRa Provide a Realistic Alternative?Muscles (Basel, Switzerland) · 2025Review
- From fibro/adipogenic progenitors to adipocytes: Understanding adipogenesis in muscle degeneration for disease modulation.The Journal of physiology · 2025Review
- Integrative Transcriptomic and Network-Based Analysis of Neuromuscular Diseases.International journal of molecular sciences · 2025Article
- Translating Muscle RNAseq Into the Clinic for the Diagnosis of Muscle Diseases.Annals of clinical and translational neurology · 2025Article
- Repurposed Nrf2 activator dimethyl fumarate rescues muscle inflammation and fibrosis in an aggravated mdx mouse model of Duchenne muscular dystrophy.Redox biology · 2025Article
- Muscle stem cells in Duchenne muscular dystrophy exhibit molecular impairments and altered cell fate trajectories impacting regenerative capacity.Cell death & disease · 2025Article
- The skeletal muscle response to high-intensity training assessed by single-nucleus RNA-sequencing is blunted in individuals with type 2 diabetes.The Journal of physiology · 2025Article
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Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy is a genetic disease produced by mutations in the dystrophin gene characterized by early onset muscle weakness leading to severe and irreversible disability. The cellular and molecular consequences of the lack of dystrophin in humans are only partially known, which is crucial for the development of new therapies aiming to slow or stop the progression of the disease. Here we have analyzed quadriceps muscle biopsies of seven DMD patients aged 2 to 4 years old and five age and gender matched controls using single nuclei RNA sequencing (snRNAseq) and correlated the results obtained with clinical data. SnRNAseq identified significant differences in the proportion of cell population present in the muscle samples, including an increase in the number of regenerative fibers, satellite cells, and fibro-adipogenic progenitor cells (FAPs) and a decrease in the number of slow fibers and smooth muscle cells. Muscle samples from the younger patients with stable mild weakness were characterized by an increase in regenerative fibers, while older patients with moderate and progressive weakness were characterized by loss of muscle fibers and an increase in FAPs. An analysis of the gene expression profile in muscle fibers identified a strong regenerative signature in DMD samples characterized by the upregulation of genes involved in myogenesis and muscle hypertrophy. In the case of FAPs, we observed upregulation of genes involved in the extracellular matrix regeneration but also several signaling pathways. Indeed, further analysis of the potential intercellular communication profile showed a dysregulation of the communication profile in DMD samples identifying FAPs as a key regulator of cell signaling in DMD muscle samples. In conclusion, our study has identified significant differences at the cellular and molecular levels in the different cell populations present in skeletal muscle samples of patients with DMD compared to controls.
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