ArticleJournal of neurology2022
Comprehensive transcriptomic analysis shows disturbed calcium homeostasis and deregulation of T lymphocyte apoptosis in inclusion body myositis.
Article in Journal of neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Altered Transcriptome Signature in Primary Human Myotubes Exposed to Inclusion Body Myositis Serum: A Pilot Case Comparison of Anti-cN1A Positive and Negative Sera.Muscles (Basel, Switzerland) · 2025Article
- Ageing Signatures and Disturbed Muscle Regeneration in Muscle Proteome of Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2025Article
- NLRP3 Inflammasome Activation and Altered Mitophagy Are Key Pathways in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2025Article
- Multi-omics analysis in inclusion body myositis identifies mir-16 responsible for HLA overexpression.Orphanet journal of rare diseases · 2025Article
- NLRP3 inflammasome activation and altered mitophagy are key pathways in inclusion body myositis.medRxiv : the preprint server for health sciences · 2024Article
- Article
- Revealing myopathy spectrum: integrating transcriptional and clinical features of human skeletal muscles with varying health conditions.Communications biology · 2024Article
- Idiopathic inflammatory myopathy and non-coding RNA.Frontiers in immunology · 2023Review
- Inclusion Body Myositis and Neoplasia: A Narrative Review.International journal of molecular sciences · 2022Review
- 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
10 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveInclusion body myositis (IBM) has an unclear molecular etiology exhibiting both characteristic inflammatory T-cell activity and rimmed-vacuolar degeneration of muscle fibers. Using in-depth gene expression and splicing studies, we aimed at understanding the different components of the molecular pathomechanisms in IBM.
methodsWe performed RNA-seq on RNA extracted from skeletal muscle biopsies of clinically and histopathologically defined IBM (n = 24), tibial muscular dystrophy (n = 6), and histopathologically normal group (n = 9). In a comprehensive transcriptomics analysis, we analyzed the differential gene expression, differential splicing and exon usage, downstream pathway analysis, and the interplay between coding and non-coding RNAs (micro RNAs and long non-coding RNAs).
resultsWe observe dysregulation of genes involved in calcium homeostasis, particularly affecting the T-cell activity and regulation, causing disturbed Ca
interpretationOur analysis provides a novel understanding of the molecular mechanisms in IBM by showing a detailed dysregulation of genes involved in calcium homeostasis and its effect on T-cell functioning in IBM muscles. Loss of T-cell regulation is hypothesized to be involved in the consistent observation of no response to immune therapies in IBM patients. Our results show that loss of apoptotic control of cytotoxic T cells could indeed be one component of their abnormal cytolytic activity in IBM muscles.
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Registered trials
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