ArticleAnnals of neurology2022
Muscle Transcriptomics Shows Overexpression of Cadherin 1 in Inclusion Body Myositis.
Article in Annals of neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- 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
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- Loss of TDP-43 Splicing Repression Occurs in Myonuclei of Inclusion Body Myositis Patients.Annals of neurology · 2025Article
- NLRP3 Inflammasome Activation and Altered Mitophagy Are Key Pathways in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2025Article
- NLRP3 inflammasome activation and altered mitophagy are key pathways in inclusion body myositis.medRxiv : the preprint server for health sciences · 2024Article
- Author Response: Clinical Subgroups and Factors Associated With Progression in Patients With Inclusion Body Myositis.Neurology · 2023Article
- Identification of Unique microRNA Profiles in Different Types of Idiopathic Inflammatory Myopathy.Cells · 2023Article
- Integrated Multi-Omics Analysis for Inferring Molecular Players in Inclusion Body Myositis.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Inclusion body myositis: Update on the diagnostic and therapeutic landscape.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 3 countries.
Funding
Abstract
objectiveThis study aimed to elucidate the molecular features of inclusion body myositis (IBM).
methodsWe performed RNA sequencing analysis of muscle biopsy samples from 67 participants, consisting of 58 myositis patients with the pathological finding of CD8-positive T cells invading non-necrotic muscle fibers expressing major histocompatibility complex class I (43 IBM, 6 polymyositis, and 9 unclassifiable myositis), and 9 controls.
resultsCluster analysis, principal component analysis, and pathway analysis showed that differentially expressed genes and pathways identified in IBM and polymyositis were mostly comparable. However, pathways related to cell adhesion molecules were upregulated in IBM as compared with polymyositis and controls (p < 0.01). Notably, CDH1, which encodes the epidermal cell junction protein cadherin 1, was overexpressed in the muscles of IBM, which was validated by another RNA sequencing dataset from previous publications. Western blotting confirmed the presence of mature cadherin 1 protein in the muscles of IBM. Immunohistochemical staining confirmed the positivity for anti-cadherin 1 antibody in the muscles of IBM, whereas there was no muscle fiber positive for anti-cadherin 1 antibody in immune-mediated necrotizing myopathy, antisynthetase syndrome, and controls. The fibers stained with anti-cadherin 1 antibody did not have rimmed vacuoles or abnormal protein accumulation. Experimental skeletal muscle regeneration and differentiation systems showed that CDH1 is expressed during skeletal muscle regeneration and differentiation.
interpretationCDH1 was detected as a differentially expressed gene, and immunohistochemistry showed that cadherin 1 exists in the muscles of IBM, whereas it was rarely seen in those of other idiopathic inflammatory myopathies. Cadherin 1 upregulation in muscle could provide a valuable clue to the pathological mechanisms of IBM. ANN NEUROL 2022;91:317-328.
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