ArticleFrontiers in immunology2025
Article in Frontiers in immunology, 2025. 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
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
3 citing papers in PubMed.
- CHAC2-mediated glutathione metabolic reprogramming drives N1 polarization of bone marrow neutrophils and exacerbates inflammatory comorbidities.International journal of oral science · 2026Article
- Immunomodulatory effects of medicinal and edible plants in autoimmune diseases: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Research advances of pan-immune inflammation value in rheumatoid arthritis.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Rheumatoid arthritis (RA) is a chronic condition characterized by joint pain that significantly impairs patients' work and daily lives. The limited understanding of the pathological mechanisms underlying RA-related pain poses challenges for effective clinical pain management. Methods: This study investigates the role of neutrophils in the pathological mechanisms of RA-related pain using collagen-induced arthritis (CIA) mice and an Results: Flow cytometric analysis revealed the accumulation and activation of neutrophils in the paws of CIA mice. Furthermore, the levels of pro-inflammatory CD95 Discussion: In summary, this study offers new insights into the pathological mechanisms of RA-related pain and demonstrates that neutrophil accumulation, N1 polarization, and ROS production contribute to RA-related pain. GLSP alleviates RA-related pain by inhibiting the pro-inflammatory phenotype of neutrophils, highlighting its potential for clinical translation in the treatment of RA.
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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.