ArticleBrain : a journal of neurology2008
Interrelation of inflammation and APP in sIBM: IL-1 beta induces accumulation of beta-amyloid in skeletal muscle.
Article in Brain : a journal of neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.
- Paraneoplastic Syndromes in Gallbladder Cancer: A Systematic Review.Medicina (Kaunas, Lithuania) · 2025Pooled it
- Cytokine inhibition in chronic fatigue syndrome patients: study protocol for a randomized controlled trial.Trials · 2015Trial
- Effect of Alemtuzumab (CAMPATH 1-H) in patients with inclusion-body myositis.Brain : a journal of neurology · 2009Trial
- Article
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Human induced pluripotent stem cell-derived myotubes to model inclusion body myositis.Acta neuropathologica communications · 2025Article
- Clinical Significance and Correlation of Plasma D-Dimer, Fibrinogen, and Cytokines in Idiopathic Inflammatory Myopathy.International journal of general medicine · 2025Article
- Article
- Current biomarkers in inclusion body myositis.Journal of neuromuscular diseases · 2024Review
- Sporadic Inclusion Body Myositis at the Crossroads between Muscle Degeneration, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- Mitochondrial defects in sporadic inclusion body myositis-causes and consequences.Frontiers in cell and developmental biology · 2024Review
- Cytotoxic immune cells do not affect TDP-43 and p62 sarcoplasmic aggregation but influence TDP-43 localisation.Scientific reports · 2023Article
- Inflammasome in Skeletal Muscle: NLRP3 Is an Inflammatory Cell Stress Component in Inclusion Body Myositis.International journal of molecular sciences · 2023Article
- Article
- Prevalence and Mechanisms of Skeletal Muscle Atrophy in Metabolic Conditions.International journal of molecular sciences · 2023Review
- Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023Article
- Skeletal muscle fibers produce B-cell stimulatory factors in chronic myositis.Frontiers in immunology · 2023Article
- NLRP3 inflammasome up-regulates major histocompatibility complex class I expression and promotes inflammatory infiltration in polymyositis.BMC immunology · 2022Article
- The immuno-behavioural covariation associated with the treatment response to bumetanide in young children with autism spectrum disorder.Translational psychiatry · 2022Article
- Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Distinct interrelationships between inflammation and beta-amyloid-associated degeneration, the two major hallmarks of the skeletal muscle pathology in sporadic inclusion body myositis (sIBM), have remained elusive. Expression of markers relevant for these pathomechanisms were analysed in biopsies of sIBM, polymyositis (PM), dermatomyositis (DM), dystrophic and non-myopathic muscle as controls, and cultured human myotubes. By quantitative PCR, a higher upregulation was noted for the mRNA-expression of CXCL-9, CCL-3, CCL-4, IFN-gamma, TNF-alpha and IL-1 beta in sIBM muscle compared to PM, DM and controls. All inflammatory myopathies displayed overexpression of degeneration-associated markers, yet only in sIBM, expression of the mRNA of amyloid precursor protein (APP) significantly and consistently correlated with inflammation in the muscle and mRNA-levels of chemokines and IFN-gamma. Only in sIBM, immunohistochemical analysis revealed that inflammatory mediators including IL-1 beta co-localized to beta-amyloid depositions within myofibres. In human myotubes, exposure to IL-1 beta caused upregulation of APP with subsequent intracellular aggregation of beta-amyloid. Our data suggest that, in sIBM muscle, production of high amounts of pro-inflammatory mediators specifically induces beta-amyloid-associated degeneration. The observations may help to design targeted treatment strategies for chronic inflammatory disorders of the skeletal muscle.
Indexed as
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.