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October 2, 2025Biomedical ReportsOpen Access

Proteomic analysis identifies novel molecular signatures and immune-metabolic pathways in rheumatoid arthritis-associated interstitial lung disease

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Authors

WCWei CuiHebei University of Engineering YZYan ZhangNanjing University of Chinese Medicine QYQingsong YeWuhan University

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Implication

Multi-center cohort study uncovers 20 dysregulated serum proteins in rheumatoid arthritis-associated interstitial lung disease, highlighting the insulin-PI3K-Akt axis as a therapeutic target.

Key Points

To identify circulating serum protein signatures and underlying immune-metabolic pathways in rheumatoid arthritis-associated interstitial lung disease to guide targeted therapeutic strategies.
Conducted a multi-center cohort study profiling pooled serum from patients with RA-ILD (n=40), patients with RA without ILD (n=40), and healthy controls (n=7).
Screened 440 candidate proteins using a high-throughput antibody array, filtering differentially expressed proteins using statistical criteria of P<0.05 and fold change >1.2 or <0.83.
Conducted functional enrichment analyses using Gene Ontology and KEGG, along with protein-protein interaction network modeling to identify central signaling hubs.
Identified 20 serum proteins demonstrating stepwise increases across groups, with expression lowest in healthy controls, higher in RA, and highest in RA-ILD (P<0.05, fold change >1.2).
Enrichment analyses highlighted cytokine-cytokine receptor interactions and PI3K-Akt signaling, with insulin emerging as a central network hub interacting with IGF-1R, IL-7, and profibrotic regulators.
Identified novel candidate biomarkers previously unlinked to RA-ILD, including CA9, EDA-A2, Gas1, CRTAM, IL-2Rb, and IL-31.

Cite This Study

Cui et al. (2025) studied this question.

synapsesocial.com/papers/6aae2eb49ff96d8fbaadbb44 https://doi.org/10.3892/br.2025.2065

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Implication

Multi-center cohort study uncovers 20 dysregulated serum proteins in rheumatoid arthritis-associated interstitial lung disease, highlighting the insulin-PI3K-Akt axis as a therapeutic target.