ArticleJournal of orthopaedic translation2025
NLRP3 inflammasome impairs fracture repair in Rheumatoid arthritis through RhoA/Rac1-IL1β axis-mediated suppression of osteoblast differentiation.
Article in Journal of orthopaedic translation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Physicochemically-guided immunomodulatory biomaterials for regulating immune responses in rheumatoid arthritis.Materials today. Bio · 2026Article
- Farnesol, the farnesol pathway, and the immune-gut-brain axis.Frontiers in pharmacology · 2026Review
- From scientific discovery to orthopaedic clinical innovation.Journal of orthopaedic translation · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Rheumatoid arthritis (RA) is often characterized by bone loss and fragility fractures and is a frequent comorbidity. The NLRP3 inflammasome drives inflammatory processes that fundamentally accompany the pathogenesis of RA. However, the role of NLRP3 inflammasome in RA fracture healing remains unclear. Methods: For Results: TNF Conclusions: Collectively, these findings suggest that NLRP3 inflammasome activation drives impaired fracture healing in RA through RhoA/Rac1‒IL-1β axis-mediated suppression of osteoblast differentiation, and pharmacologic inhibition with MCC950 effectively rescues delayed fracture healing in RA mouse model. The Translational Potential of this Article: This study provides novel insights into the mechanisms underlying delayed fracture healing in RA and highlights the potential therapeutic benefits of targeting the NLRP3 inflammasome.
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Registered trials
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