ArticleMediators of inflammation2025
Integrative Bulk and Single-Cell Transcriptomic Profiling Reveals Oxidative Stress-Related Genes and Potential Therapeutic Targets in Osteoarthritis.
Article in Mediators of inflammation, 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.
- Oxidative-Stress-Associated Molecular Signatures in Immune-Mediated Diseases: A Systematic Review Integrating Machine Learning and Systems Biology Approaches.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is increasingly recognized as a degenerative joint disease that leads to a serious problem of public health, yet the underlying molecular mechanisms remain incompletely understood. In this study, we integrated bulk and single-cell RNA sequencing (scRNA-seq) datasets from the Gene Expression Omnibus (GEO) to systematically investigate oxidative stress-related genes and pathways in OA. Gene set enrichment analysis (GSEA) revealed significant activation of oxidative stress signaling in OA cartilage tissues, with 58 differentially expressed oxidative stress-related genes identified. Subsequent LASSO regression analysis highlighted seven diagnostic genes (STC2, LSP1, COL6A1, FOS, SELENON, TP53, and HSPA8), which demonstrated robust diagnostic performance in both training and validation cohorts. Single-cell analysis further revealed cell-type-specific differences in oxidative stress activity, with homeostatic chondrocytes (HomCs) exhibiting the highest pathway scores. Among the identified genes, FOS emerged as a hub regulator, showing elevated expression in HomCs from OA samples and strong associations with immune infiltration and proinflammatory pathways. Functional assays demonstrated that FOS knockdown significantly attenuated IL-1β-induced oxidative stress, apoptosis, and inflammatory cytokine (interleukin-6 [IL-6] and tumor necrosis factor-alpha [TNF-α]) release in chondrocytes. Furthermore, molecular docking and dynamics simulations identified ursolic acid (UA) as a stable small-molecule FOS binder, and in vitro experiments confirmed its inhibitory effects on oxidative stress and inflammation, comparable to FOS silencing or pharmacological inhibition. Collectively, our findings suggest that oxidative stress-related genes, particularly FOS, play a central role in OA pathogenesis by linking redox imbalance to immune dysregulation and chondrocyte injury, and highlight UA as a potential therapeutic candidate for OA management.
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.