Identification of biomarkers related to neutrophil extracellular traps and potential therapeutic drugs for rheumatoid arthritis using computational analysis

利用计算机分析鉴定与中性粒细胞胞外陷阱相关的生物标志物和类风湿性关节炎的潜在治疗药物

阅读:1

Abstract

BACKGROUND: Neutrophil extracellular traps (NETs) derived from neutrophils are implicated in the pathogenesis of rheumatoid arthritis (RA) pathogenicity, though the underlying mechanisms remain unclear. METHODS: Data were obtained from Gene Expression Omnibus (GEO) database. First, Gene Set Variation Analysis (GSVA) was used to calculate NET scores, and ConsensusClusterPlus was employed to classify RA samples. Subsequently, weighted gene co-expression network analysis (WGCNA) was used to construct co-expression networks. Lasso regression and support vector machine recursive feature elimination (SVM-RFE) were then used to cross-screen biomarkers for RA, with predictive performance evaluated via the timeROC package. Immune infiltration in RA samples was assessed using ssGSEA and MCPcounter methods. Additionally, qRT-PCR was conducted to validate the expression of key genes. Finally, potential therapeutic drugs were predicted through Enrichr using the DSigDB database, and candidate compounds were preprocessed with PyMOL and ChemBioOffice before molecular docking with AutoDockTools. RESULTS: RA patients had significantly higher NET scores than controls, and the samples were divided into C1 and C2. WGCNA combined with differential analysis identified eight key genes, and five biomarkers were screened by two machine learning algorithms, namely, ANGPTL1, CASP8, FNIP2, MEOX2, and ZNF780B. Both the training set and validation set showed an AUC > 0.7. Immunological analysis revealed an association with neutrophil infiltration, while drug prediction and molecular docking revealed that N-Acetyl-L-cysteine and Eckol exhibited favorable binding activity. CONCLUSION: This study provided novel insights into RA progression based on NETs, offering potential signature genes for the prognostic prediction of RA.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。