ReviewFrontiers in immunology2024
Inflammasomes and idiopathic inflammatory myopathies.
Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- The Role and Potential Mechanism of Pectin and Pectin Oligosaccharides in Treating Intestinal Inflammation by Regulating Gut Microbiota.Probiotics and antimicrobial proteins · 2026Review
- Tryptophan metabolism mediated by the gut microbiota inhibits pyroptosis via the AhR signaling pathway to maintain intestinal epithelial homeostasis.Microbiome · 2026Article
- Disease activity and immune disbalance are key drivers of infections in patients with idiopathic inflammatory myopathies: results from the MYOTReCSZ cohort.Immunologic research · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic inflammatory myopathies (IIM) are a group of systemic autoimmune diseases characterized by muscle weakness and elevated serum creatine kinase levels. Recent research has highlighted the role of the innate immune system, particularly inflammasomes, in the pathogenesis of IIM. This review focuses on the role of inflammasomes, specifically NLRP3 and AIM2, and their associated proteins in the development of IIM. We discuss the molecular mechanisms of pyroptosis, a programmed cell death pathway that triggers inflammation, and its association with IIM. The NLRP3 inflammasome, in particular, has been implicated in muscle fiber necrosis and the subsequent release of damage-associated molecular patterns (DAMPs), leading to inflammation. We also explore the potential therapeutic implications of targeting the NLRP3 inflammasome with inhibitors such as glyburide and MCC950, which have shown promise in reducing inflammation and improving muscle function in preclinical models. Additionally, we discuss the role of caspases, particularly caspase-1, in the canonical pyroptotic pathway associated with IIM. The understanding of these mechanisms offers new avenues for therapeutic intervention and a better comprehension of IIM pathophysiology.
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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.