ReviewAnnals of clinical and translational neurology2017
Immune and myodegenerative pathomechanisms in inclusion body myositis.
Review in Annals of clinical and translational neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- The NORAD-Pumilio regulatory axis in the evolution of inclusion body myositis.Journal of neuropathology and experimental neurology · 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
- Idiopathic Inflammatory Myopathy-Molecular Mechanisms Underlying Its Pathogenesis and Physical Therapy Effects.International journal of molecular sciences · 2025Review
- Multi-omics analysis in inclusion body myositis identifies mir-16 responsible for HLA overexpression.Orphanet journal of rare diseases · 2025Article
- Inclusion body myositis, viral infections, and TDP-43: a narrative review.Clinical and experimental medicine · 2024Review
- Cytotoxic immune cells do not affect TDP-43 and p62 sarcoplasmic aggregation but influence TDP-43 localisation.Scientific reports · 2023Article
- Serum-Circulating microRNAs in Sporadic Inclusion Body Myositis.International journal of molecular sciences · 2023Article
- Inflammasome in Skeletal Muscle: NLRP3 Is an Inflammatory Cell Stress Component in Inclusion Body Myositis.International journal of molecular sciences · 2023Article
- Potential common molecular mechanisms between Sjögren syndrome and inclusion body myositis: a bioinformatic analysis andFrontiers in immunology · 2023Article
- Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023Article
- Inclusion Body Myositis and Neoplasia: A Narrative Review.International journal of molecular sciences · 2022Review
- Pathophysiological Mechanisms and Treatment of Dermatomyositis and Immune Mediated Necrotizing Myopathies: A Focused Review.International journal of molecular sciences · 2022Review
- Review
- Muscle Transcriptomics Shows Overexpression of Cadherin 1 in Inclusion Body Myositis.Annals of neurology · 2022Article
- Loss of TDP-43 function and rimmed vacuoles persist after T cell depletion in a xenograft model of sporadic inclusion body myositis.Science translational medicine · 2022Article
- An Overview of Mitochondrial Protein Defects in Neuromuscular Diseases.Biomolecules · 2021Review
- Myo-Inositol Transporter SLC5A3 Associates with Degenerative Changes and Inflammation in Sporadic Inclusion Body Myositis.Biomolecules · 2020Article
- A cross-sectional study of hand function in inclusion body myositis: Implications for functional rating scale.Neuromuscular disorders : NMD · 2020Observational
- Comparative Genomic Insights into Secondary Metabolism Biosynthetic Gene Cluster Distributions of MarineMarine drugs · 2019Article
- Trial of canakinumab, an IL-1β receptor antagonist, in patients with inclusion body myositis.Neurology(R) neuroimmunology & neuroinflammation · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inclusion Body Myositis (IBM) is a relatively common acquired inflammatory myopathy in patients above 50 years of age. Pathological hallmarks of IBM are intramyofiber protein inclusions and endomysial inflammation, indicating that both myodegenerative and inflammatory mechanisms contribute to its pathogenesis. Impaired protein degradation by the autophagic machinery, which regulates innate and adaptive immune responses, in skeletal muscle fibers has recently been identified as a potential key pathomechanism in IBM. Immunotherapies, which are successfully used for treating other inflammatory myopathies lack efficacy in IBM and so far no effective treatment is available. Thus, a better understanding of the mechanistic pathways underlying progressive muscle weakness and atrophy in IBM is crucial in identifying novel promising targets for therapeutic intervention. Here, we discuss recent insights into the pathomechanistic network of mutually dependent inflammatory and degenerative events during IBM.
Identifiers
What OpenQuestion holds
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.