ArticleScientific reports2025
Identification and validation of oxidative stress signature genes in the trabecular meshwork of glaucoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Edaravone Attenuates Retinal Ganglion Cell Ferroptosis Induced by Ischemia Reperfusion via Inhibiting the p38 MAPK/ATF3 Signaling Pathway.Molecular neurobiology · 2026Article
- Oxidative Stress in Glaucoma: From Pathogenic Mechanisms to Emerging Antioxidant Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Electrochemical Biosensors for Exosome Detection: Current Advances, Challenges, and Prospects for Glaucoma Diagnosis.Sensors (Basel, Switzerland) · 2026Review
- Experimental models to study oxidative stress in glaucoma: integratingFrontiers in pharmacology · 2026Review
- Aggregate index of systemic inflammation and glaucoma status: population-based evidence with clinical validation.Frontiers in medicine · 2026Article
- Role of reactive oxygen species and oxidative stress in the pathomechanism of glaucoma.Medical hypothesis, discovery & innovation ophthalmology journal · 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
3 authors.
Funding
Abstract
Oxidative stress (OS) plays an important role in trabecular meshwork (TM) dysfunction in glaucoma, but its molecular mechanism remains unclear. We integrated the GSE27276 dataset and OS-related gene sets from GeneCards to screen 61 differentially expressed OS-related genes (DEOSGs). Functional enrichment analysis revealed that these genes are primarily involved in inflammatory and OS-related signaling pathways, including IL-17, TNF, and NF-κB. A protein-protein interaction (PPI) network constructed via the STRING database identified seven hub genes (CCL3, CXCL1, NFKBIA, VCAM1, LCN2, TNFRSF1A, and HP). Validation using the GSE124114, GSE37474, and GSE65240 datasets showed that the expression of CXCL1 and VCAM1 was downregulated, while NFKBIA was upregulated. Additionally, all three genes exhibited an area under the curve (AUC) greater than 0.7. Immune infiltration analysis demonstrated significant associations between these genes and immune cells, particularly regulatory T cells and neutrophils. Regulatory network analysis suggested that transcription factors (RELA, NFKB1) and microRNAs (hsa-miR-34a-5p) may modulate these core genes. Drug-gene interaction studies identified 35 potential therapeutic agents, including Infliximab and Vitamin B6. This study systematically elucidates the molecular mechanisms of OS in glaucoma, proposing that the identified core genes and their regulatory networks not only serve as novel biomarkers for diagnosis but also provide a theoretical foundation for developing targeted therapeutic strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.