ArticleInternational journal of molecular sciences2023
Inflammasome in Skeletal Muscle: NLRP3 Is an Inflammatory Cell Stress Component in Inclusion Body Myositis.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Pathological changes and therapeutic strategies for sarcopenia.EFORT open reviews · 2026Review
- Amelioration of contusion-induced muscle injury via regulation of the NLRP3 inflammasome.International journal of medical sciences · 2026Article
- 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
- NLRP3 inflammasome activation and altered mitophagy are key pathways in inclusion body myositis.medRxiv : the preprint server for health sciences · 2024Article
- Sporadic Inclusion Body Myositis at the Crossroads between Muscle Degeneration, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- NLRP3 Contributes to Sarcopenia Associated to Dependency Recapitulating Inflammatory-Associated Muscle Degeneration.International journal of molecular sciences · 2024Article
- Inflammasomes and idiopathic inflammatory myopathies.Frontiers in immunology · 2024Review
- Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Inclusion body myositis (IBM) is a chronic, mostly treatment-resistant, inflammatory myopathy with a pathology that centers around specific interactions between inflammation and protein accumulation. The study aimed to identify the inflammasome as a key event in the complex network of pathomechanisms. Regulation of the inflammasome was assessed in a well-established pro-inflammatory cell culture model using human myoblasts and primary human myotubes. By quantitative PCR, western blot and immunocytochemistry, inflammasome markers including NLRP3 were assessed in muscle cells exposed to the cytokines IL-1β and IFN-γ. The data were corroborated by analysis of muscle biopsies from patients with IBM compared to other myositis subtypes. In the cell culture model of IBM, the NLRP3 inflammasome was significantly overexpressed, as evidenced by western blot (
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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.