ArticleNature aging2024
Cell type mapping of inflammatory muscle diseases highlights selective myofiber vulnerability in inclusion body myositis.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- An integrated reference atlas of human skeletal muscle.EBioMedicine · 2026Article
- Myeloid dendritic cell subsets characterise muscle in patients with inclusion body myositis and correlate with the IFN-γ pathway and effector T cell markers.Annals of the rheumatic diseases · 2026Article
- Oligodendrocyte Piezo2 is a regulator of age-dependent myelin integrity and dysregulated in multiple sclerosis.Communications biology · 2026Article
- Inflammation reprograms fibro-adipogenic progenitors to sustain immunopathogenic niches in myositis.Cell death & disease · 2026Article
- Ectopic co-expression of canonical and LINE1 and THE1A-exonizing IL23R transcripts in sarcoid myopathy.Journal of human genetics · 2026Article
- High-plex spatial protein profiling of skeletal muscle biopsies in inflammatory myopathies using the MACSima™ imaging platform: A pilot study.Acta neuropathologica communications · 2026Article
- Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.Journal of advanced research · 2026Review
- Spatial protein expression patterns across pathologically-associated fibers revealed molecular specialization in inclusion body myositis.Cell communication and signaling : CCS · 2026Article
- Proteomic profiles in inclusion body myositis and polymyositis with mitochondrial pathology.Acta neuropathologica communications · 2026Article
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Spatially Resolved Profiling of Compartmentalized Muscle and Brain Inflammation.European journal of immunology · 2025Review
- Aquaporin-4 downregulation in dysphagic patients with idiopathic inflammatory myopathies: myofiber vulnerability and inflammation drivers.Rheumatology (Oxford, England) · 2025Article
- Recent advances in immunological mechanisms and murine disease models of idiopathic inflammatory myopathies.Inflammation and regeneration · 2025Review
- Mitochondria-centred metabolomic map of inclusion body myositis: sex-specific alterations in central carbon metabolism.Annals of the rheumatic diseases · 2025Article
- Article
- Loss of TDP-43 Splicing Repression Occurs in Myonuclei of Inclusion Body Myositis Patients.Annals of neurology · 2025Article
- In situ spatial transcriptomic analysis of human skeletal muscle using the Xenium platform.Cell and tissue research · 2025Article
- Spatial transcriptomics in autoimmune rheumatic disease: potential clinical applications and perspectives.Inflammation and regeneration · 2025Review
- Factors, mechanisms and improvement methods of muscle strength loss.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Inclusion body myositis (IBM) is the most prevalent inflammatory muscle disease in older adults with no effective therapy available. In contrast to other inflammatory myopathies such as subacute, immune-mediated necrotizing myopathy (IMNM), IBM follows a chronic disease course with both inflammatory and degenerative features of pathology. Moreover, causal factors and molecular drivers of IBM progression are largely unknown. Therefore, we paired single-nucleus RNA sequencing with spatial transcriptomics from patient muscle biopsies to map cell-type-specific drivers underlying IBM pathogenesis compared with IMNM muscles and noninflammatory skeletal muscle samples. In IBM muscles, we observed a selective loss of type 2 myonuclei paralleled by increased levels of cytotoxic T and conventional type 1 dendritic cells. IBM myofibers were characterized by either upregulation of cell stress markers featuring GADD45A and NORAD or protein degradation markers including RNF7 associated with p62 aggregates. GADD45A upregulation was preferentially seen in type 2A myofibers associated with severe tissue inflammation. We also noted IBM-specific upregulation of ACHE encoding acetylcholinesterase, which can be regulated by NORAD activity and result in functional denervation of myofibers. Our results provide promising insights into possible mechanisms of myofiber degeneration in IBM and suggest a selective type 2 fiber vulnerability linked to genomic stress and denervation pathways.
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