ArticlePeerJ2025
Exploring differential gene expression and biomarker potential in systemic lupus erythematosus: a retrospective study.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Extracellular Vesicles of Streptococcus anginosus Mediate Gastritis via Epithelial Barrier Disruption and Macrophage-driven Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by inflammation and immune-mediated multi-organ system damage, accompanied by clinical manifestations such as fever, hair loss, skin rash, oral ulcers, and joint pain and swelling. SLE has been reported to affect more than 3.4 million people worldwide, of which approximately 90% are women. Purpose: This study aims to identify and characterize key hub genes implicated in SLE through comprehensive bioinformatics analyses, providing a theoretical foundation for the development of more effective therapeutic strategies. Methods: Two datasets were procured from the Gene Expression Omnibus (GEO) database: GSE13887 and GSE10325. Differentially expressed genes (DEGs) were identified and subjected to functional enrichment analysis, protein-protein interaction (PPI) network construction, and receiver operating characteristic (ROC) curve analysis to evaluate potential hub genes. The top 20 significantly upregulated and downregulated DEGs, alongside the top 15 enriched Gene Ontology (GO) terms and five Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, were screened from both datasets. Quantitative real-time PCR (RT-q PCR) was utilized to validate hub gene expression in CD3 + T cells from peripheral blood samples of SLE patients. Concurrently, flow cytometry was employed to quantify inflammatory cytokines in peripheral blood samples. Results: Bioinformatics analyses identified 1,912 DEGs in GSE13887 and 52 DEGs in GSE10325, with eight DEGs common to both datasets. Functional enrichment analysis underscored critical biological processes, notably cell-mediated cytotoxicity and cell killing. PPI network and enrichment analyses highlighted seven hub genes, among which Conclusions: FCER1A and RGS1 are significantly associated with SLE and serve as potential biomarkers for distinguishing SLE patients from healthy individuals. Their involvement in SLE pathogenesis underscores their potential as targets for future diagnostic and therapeutic interventions.
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.