ArticleFrontiers in immunology2025
Integrated multi-omics for potential biomarkers and molecular mechanism of persistent inflammatory refractory rheumatoid arthritis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Immunological heterogeneity in rheumatoid arthritis: challenges in early-stage stratification, non-response to targeted therapy, and the restoration of immune tolerance.Frontiers in immunology · 2026Review
- Luteolin-7-O-rutinoside alleviates rheumatoid arthritis through downregulation of the PI3K/AKT/NF-κB and cell cycle signaling pathways.Frontiers in pharmacology · 2026Article
- Precision medicine in rheumatoid arthritis: advances and clinical applications of multi-omics biomarkers.Frontiers in immunology · 2026Review
- GeneCytNet: an interpretable deep learning framework for rheumatoid arthritis classification andFrontiers in immunology · 2026Article
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Authors and funding
6 authors.
Funding
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Abstract
Introduction: Persistent inflammatory refractory rheumatoid arthritis (PIRRA) presents a major clinical challenge, and its underlying molecular mechanisms remain inadequately understood. Methods: athogenesis. Synovial joint tissues were collected from 30 TgTC mice and 30 Friend virus B (FVB) control mice. Of these, 18 mice per group were used for transcriptomic, proteomic, and metabolomic analyses; 6 for pathological examination and microCT imaging; and 6 for validation experiments. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, protein-protein interaction networks, and KEGG Markup Language (KGML) network analysis were employed to characterize the functional roles of differentially expressed genes (DEGs), proteins, metabolites, and associated biological pathways. Notably, five genes/proteins-macrophage-expressed gene 1 ( Results: A total of 2,410 DEGs, 366 differentially expressed proteins, and 120 significantly altered metabolites (P < 0.05) were identified between the model (TgTC ) and control (FVB) groups. These molecules were mainly associated with Golgi apparatus dysfunction, lipid metabolism, and immune-inflammatory responses. Integrative multi-omics analysis further revealed that these molecular alterations are involved in the activation of the PI3K-AKT-mTOR signaling pathway, as well as disruptions in tryptophan and lipid metabolism. Among the metabolites, phosphatidylinositol (PI) (12:0/12:0), N-docosahexaenoyl tryptophan, and PI (22:1(11Z)/0:0) were identified as key metabolic signatures of persistent joint synovitis in TgTC mice. In addition, the expression of Discussion: Our findings highlight the critical role of altered gene, protein, and metabolite expression in the pathogenesis of PIRRA, offering new insights into its molecular basis and potential therapeutic targets.
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