ArticleCommunications biology2022
Single nuclei transcriptomics of muscle reveals intra-muscular cell dynamics linked to dystrophin loss and rescue.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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
32 citing papers in PubMed, 40 citations in OpenAlex.
- GDF5 modulation of MuSC pool as a potential therapeutic benefit for DMD.Molecular therapy. Nucleic acids · 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
- Meeting report: 2025 muscular dystrophy association summit on 'safety and challenges in gene therapy of neuromuscular diseases'.Journal of neuromuscular diseases · 2026Article
- ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD).Nature communications · 2026Article
- Picalm coordinates clathrin-mediated endocytosis and actin remodeling during myogenesis.Molecular metabolism · 2026Article
- Single nuclei/cell transcriptomics reveal DMD driven cell dynamics and mechanisms of fibroblast inflammatory tissue priming in human dystrophic muscle.Research square · 2026Article
- Transcriptomics-based analysis of muscle injury mechanism mediated by inflammatory imbalance in the Duchenne muscular dystrophy muscle microenvironment.Frontiers in neurology · 2026Article
- Macrophage plasticity and metabolic control in muscle repair and disease.Frontiers in immunology · 2026Review
- Heterogeneous Macrophage Activation in Acute Skeletal Muscle Sterile Injury andInternational journal of molecular sciences · 2025Article
- Optimized upstream analytical workflow for single-nucleus transcriptomics in main metabolic tissues.Life metabolism · 2025Article
- GsMTx4-blocked PIEZO1 channel promotes myogenic differentiation and alleviates myofiber damage in Duchenne muscular dystrophy.Skeletal muscle · 2025Article
- Inhibiting EZH2 complements steroid effects in Duchenne muscular dystrophy.Science advances · 2025Article
- Trajectory Inference for Single Cell Omics.ArXiv · 2025Article
- Skeletal muscle stem cells modulate niche function in Duchenne muscular dystrophy mouse through YY1-CCL5 axis.Nature communications · 2025Article
- Comprehensive profiling of chemokine and NETosis-associated genes in sarcopenia: construction of a machine learning-based diagnostic nomogram.Frontiers in medicine · 2025Article
- Cell fusion dynamics: mechanisms of multinucleation in osteoclasts and macrophages.Inflammation and regeneration · 2024Review
- Beyond the bulk: overview and novel insights into the dynamics of muscle satellite cells during muscle regeneration.Inflammation and regeneration · 2024Review
- Spatiotemporal transcriptomic mapping of regenerative inflammation in skeletal muscle reveals a dynamic multilayered tissue architecture.The Journal of clinical investigation · 2024Article
- Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
In Duchenne muscular dystrophy, dystrophin loss leads to chronic muscle damage, dysregulation of repair, fibro-fatty replacement, and weakness. We develop methodology to efficiently isolate individual nuclei from minute quantities of frozen skeletal muscle, allowing single nuclei sequencing of irreplaceable archival samples and from very small samples. We apply this method to identify cell and gene expression dynamics within human DMD and mdx mouse muscle, characterizing effects of dystrophin rescue by exon skipping therapy at single nuclei resolution. DMD exon 23 skipping events are directly observed and increased in myonuclei from treated mice. We describe partial rescue of type IIa and IIx myofibers, expansion of an MDSC-like myeloid population, recovery of repair/remodeling M2-macrophage, and repression of inflammatory POSTN1 + fibroblasts in response to exon skipping and partial dystrophin restoration. Use of this method enables exploration of cellular and transcriptomic mechanisms of dystrophin loss and repair within an intact muscle environment. Our initial findings will scaffold our future work to more directly examine muscular dystrophies and putative recovery pathways.
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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.