ArticleToxicology research2025
Network toxicology and immune-metabolic dysregulation: linking per- and polyfluoroalkyl substances exposure to osteoarthritis pathogenesis.
Article in Toxicology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Exploring the Toxicological Effects of Acetyl Tributyl Citrate Exposure on Osteoarthritis Based on Machine Learning, Network Toxicology and Molecular Docking Analysis.Open access rheumatology : research and reviews · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Per- and polyfluoroalkyl substances (PFAS) are emerging environmental contaminants linked to various health conditions. However, the molecular mechanisms by which PFAS contribute to OA remain unclear. This study integrates network toxicology and bioinformatics to explore PFAS-related toxicity targets and their roles in OA pathogenesis. Transcriptomic data from the GSE48556 dataset were analyzed to identify differentially expressed genes (DEGs). PFAS-related genes (PSRGs) were retrieved from the CTD. Cross-analysis revealed overlapping genes, which were further evaluated via protein-protein interaction (PPI) networks, pathway enrichment, immune infiltration analysis, and nomogram construction. A total of 1,703 DEGs (910 upregulated, 793 downregulated) were identified in OA. Cross-analysis with 346 PSRGs yielded 26 overlapping genes, highlighting PFAS-OA molecular links. Enrichment analysis implicated IL-17 signaling, Th1/Th2 differentiation, and fatty acid metabolism as key pathways disrupted by PFAS. Immune-inflammatory pathways were robustly enriched, with CD3E, CARD11, and IFNG driving synovial inflammation. A nomogram incorporating five core targets (CARD11, IFNG, PAX8, PLD1, ZNF609) predicted OA risk and demonstrated clinical utility via decision curve analysis. Immune profiling revealed elevated infiltration of T cells, Th1 cells, and NK CD56dim cells in OA, alongside upregulated antigen presentation and TCR/BCR signaling. Core PFAS-related targets correlated significantly with immune dysregulation. PFAS exposure exacerbates OA by dysregulating immune-inflammatory axes and metabolic pathways, promoting synovitis and cartilage degradation. The identified genetic targets and nomogram provide mechanistic insights and translational tools for OA risk prediction in PFAS-exposed populations. This study establishes a systems-level framework linking PFAS toxicity to OA progression, offering actionable targets for therapeutic intervention.
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.