ArticleiScience2022
Single cell sequencing maps skeletal muscle cellular diversity as disease severity increases in dystrophic mouse models.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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Who cites it
44 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- Excess muscle plasma membrane leak disrupts ECM content and shifts macrophage-mediated muscle repair.JCI insight · 2026Article
- Mesenchymal Stromal Cell-Mediated Intercellular Communication: Mapping the Interactome for Skeletal Muscle Homeostasis and Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell and spatial transcriptomic profiling reveals distinct immune landscapes in murine lungs infected with H1N1 versus H5N1 influenza viruses.Journal of virology · 2026Article
- Collagen VI is a fibrosis-associated signal disrupting muscle regeneration across distinct human myopathies.EMBO reports · 2026Article
- Unraveling the spatial landscape of dystrophinopathies: a transcriptomic approach to Becker and Duchenne muscular dystrophies.The Journal of pathology · 2026Article
- Fibroadipogenic progenitor-secreted prostaglandin E2 coordinates stem cell fate via autocrine and paracrine crosstalk in healthy and dystrophic muscle.Cell death and differentiation · 2026Article
- Single-cell transcriptomics highlights macrophage-driven regulation of EndMT and repair in injured muscle.Communications biology · 2026Article
- Single-Cell RNA-Sequencing Reveals Cachectic Satellite Cell Population in Muscle of Male Mice With Cancer Cachexia.Journal of cachexia, sarcopenia and muscle · 2026Article
- Targeting Skeletal Muscle in Duchenne Muscular Dystrophy: Integrating in Silico and Experimental Approaches to Sodium-Glucose Cotransporter-2 Inhibition.The American journal of pathology · 2026Article
- Macrophage Infiltration, Activation, and Therapeutic Implication in Skeletal Muscle Injury and Repair.International journal of molecular sciences · 2026Review
- Impaired stem cell migration and divisions in Duchenne muscular dystrophy revealed by live imaging.Nature communications · 2026Article
- Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Disease exacerbation in human DMD MYOrganoids enables gene therapy evaluation and unveils persistence of fibrotic activity.NPJ Regenerative medicine · 2026Article
- Stereo-cell coupled with single-cell transcriptomics identifies a transitional metabolic state in maturing skeletal muscle myofibers.Frontiers in genetics · 2026Article
- (Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective.Degenerative neurological and neuromuscular disease · 2026Review
- FAP-CAR-T cells reduce dystrophic muscle fibrosis, improving adeno-associated virus gene transfer efficacy.Molecular therapy. Methods & clinical development · 2025Article
- Roles of plasminogen activator inhibitor-1 in aging-related muscle and bone loss in mice.Aging · 2025Article
- Heterogeneous Macrophage Activation in Acute Skeletal Muscle Sterile Injury andInternational journal of molecular sciences · 2025Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is caused by out-of-frame mutations in the DMD gene resulting in the absence of a functional dystrophin protein, leading to a devastating and progressive lethal muscle-wasting disease. Little is known about cellular heterogeneity as disease severity increases. Advances in single-cell RNA sequencing (scRNA-seq) enabled us to explore skeletal muscle-resident cell populations in healthy, dystrophic, and severely dystrophic mouse models. We found increased frequencies of activated fibroblasts, fibro-adipogenic progenitor cells, and pro-inflammatory macrophages in dystrophic gastrocnemius muscles and an upregulation of extracellular matrix genes on endothelial cells in dystrophic and severely dystrophic muscles. We observed a pronounced risk of clotting, especially in the severely dystrophic mice with increased expression of plasminogen activator inhibitor-1 in endothelial cells, indicating endothelial cell impairment as disease severity increases. This work extends our understanding of the severe nature of DMD which should be considered when developing single or combinatorial approaches for 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.