Identification the role of necroptosis in rheumatoid arthritis by WGCNA network.
Rheumatoid arthritis
WGCNA
hub genes
immune cells
necroptosis
Journal
Autoimmunity
ISSN: 1607-842X
Titre abrégé: Autoimmunity
Pays: England
ID NLM: 8900070
Informations de publication
Date de publication:
Dec 2024
Dec 2024
Historique:
medline:
13
6
2024
pubmed:
13
6
2024
entrez:
13
6
2024
Statut:
ppublish
Résumé
Rheumatoid arthritis (RA) is the predominant manifestation of inflammatory arthritis, distinguished by an increasing burden of morbidity and mortality. The intricate interplay of genes and signalling pathways involved in synovial inflammation in patients with RA remains inadequately comprehended. This study aimed to ascertain the role of necroptosis in RA, as along with their associations with immune cell infiltration. Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were employed to identify central genes for RA. In this study, identified total of 28 differentially expressed genes (DEGs) were identified in RA. Utilising WGCNA, two co-expression modules were generated, with one module demonstrating the strongest correlation with RA. Through the integration of differential gene expression analysis, a total of 5 intersecting genes were discovered. These 5 hub genes, namely fused in sarcoma (FUS), transformer 2 beta homolog (TRA2B), eukaryotic translation elongation factor 2 (EEF2), cleavage and polyadenylation specific factor 6 (CPSF6) and signal transducer and activator of transcription 3 (STAT3) were found to possess significant diagnostic value as determined by receiver operating characteristic (ROC) curve analysis. The close association between the concentrations of various immune cells is anticipated to contribute to the diagnosis and treatment of RA. Furthermore, the infiltration of immune cells mentioned earlier is likely to exert a substantial influence on the initiation of this disease.
Identifiants
pubmed: 38869013
doi: 10.1080/08916934.2024.2358069
doi:
Substances chimiques
STAT3 Transcription Factor
0
Biomarkers
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM