ArticleProceedings of the National Academy of Sciences of the United States of America2020
Degenerative and regenerative pathways underlying Duchenne muscular dystrophy revealed by single-nucleus RNA sequencing.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 147 citations in OpenAlex.
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
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- Excess muscle plasma membrane leak disrupts ECM content and shifts macrophage-mediated muscle repair.JCI insight · 2026Article
- Unraveling the spatial landscape of dystrophinopathies: a transcriptomic approach to Becker and Duchenne muscular dystrophies.The Journal of pathology · 2026Article
- BCL6 regulates skeletal muscle mass and mitochondrial bioenergetics.Molecular metabolism · 2026Article
- In vitro-reconstituted Drosophila Arc capsids deliver gene editors to dystrophic muscle.bioRxiv : the preprint server for biology · 2026Article
- Identification of biomarkers associated with pathological dynamic progression in dystrophinopathies.Scientific reports · 2026Article
- ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD).Nature communications · 2026Article
- Single nuclei/cell transcriptomics reveal DMD driven cell dynamics and mechanisms of fibroblast inflammatory tissue priming in human dystrophic muscle.Research square · 2026Article
- RUNX2 Activation in Fibro/Adipogenic Progenitors Promotes Muscle Fibrosis in Muscular Dystrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Profiling the epigenomic landscape of late embryonic and adult mouse hind limb muscles.Scientific reports · 2026Article
- Coiled-coil heterodimer-mediated split base editing systems enable flexible and robust nucleotide substitutions.Nature communications · 2026Article
- Stereo-cell coupled with single-cell transcriptomics identifies a transitional metabolic state in maturing skeletal muscle myofibers.Frontiers in genetics · 2026Article
- Transcriptomics-based analysis of muscle injury mechanism mediated by inflammatory imbalance in the Duchenne muscular dystrophy muscle microenvironment.Frontiers in neurology · 2026Article
- Conditional Dmd ablation in muscle and brain causes profound effects on muscle function and neurobehavior.Communications biology · 2025Article
- The multimodal transcriptional response of denervated skeletal muscle involves regulation ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Transcriptomic profiling of skeletal muscle in the DMDScientific reports · 2025Article
- Liposome-Enabled Nanomaterials for Muscle Regeneration.Small methods · 2025Review
- Article
50 more citing papers are in PubMed but not listed here.
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7 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a fatal muscle disorder characterized by cycles of degeneration and regeneration of multinucleated myofibers and pathological activation of a variety of other muscle-associated cell types. The extent to which different nuclei within the shared cytoplasm of a myofiber may display transcriptional diversity and whether individual nuclei within a multinucleated myofiber might respond differentially to DMD pathogenesis is unknown. Similarly, the potential transcriptional diversity among nonmuscle cell types within dystrophic muscle has not been explored. Here, we describe the creation of a mouse model of DMD caused by deletion of exon 51 of the dystrophin gene, which represents a prevalent disease-causing mutation in humans. To understand the transcriptional abnormalities and heterogeneity associated with myofiber nuclei, as well as other mononucleated cell types that contribute to the muscle pathology associated with DMD, we performed single-nucleus transcriptomics of skeletal muscle of mice with dystrophin exon 51 deletion. Our results reveal distinctive and previously unrecognized myonuclear subtypes within dystrophic myofibers and uncover degenerative and regenerative transcriptional pathways underlying DMD pathogenesis. Our findings provide insights into the molecular underpinnings of DMD, controlled by the transcriptional activity of different types of muscle and nonmuscle nuclei.
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