ArticleScientific reports2025
Shared pathogenic mechanisms linking obesity and idiopathic pulmonary fibrosis revealed by bioinformatics and in vivo validation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Cerium oxide nanoparticles: antioxidant properties in silicosis treatment and biomedical application prospects-a dialectical consideration.Drug delivery · 2026Review
- Exploring the anti-fibrotic effects of safflower in systemic sclerosis based on metabolomics and gut microbiota analyses.Frontiers in pharmacology · 2026Article
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Authors and funding
7 authors.
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Abstract
Previous studies have suggested a potential correlation between obesity and idiopathic pulmonary fibrosis (IPF). This study aimed to elucidate pathogenic pathways connecting obesity and IPF and identify diagnostic biomarkers for obesity-related pulmonary fibrosis. Obesity and IPF datasets were obtained through the Gene Expression Omnibus (GEO) database. Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were used to identify shared genes for obesity and IPF. Functional enrichment (GO/KEGG), protein-protein interaction (PPI) networks, and machine learning algorithms were applied to screen hub genes, validated by ROC curves. High-fat diet (HFD)-induced obese mice with bleomycin-induced pulmonary fibrosis underwent histological assessment and qRT-PCR validation. Molecular docking evaluated flavonoid binding to hub genes. We identified 128 shared genes between obesity and IPF, predominantly enriched in immune and inflammatory pathways. Machine learning prioritized three hub genes (NLRC4, SPI1, and NCF2), validated by ROC analysis (AUC > 0.7). In animal model, these genes exhibited significant upregulation, correlating with exacerbated fibrosis. Molecular docking highlighted strong binding affinities (-6.3 to -9.6 kcal/mol) between dietary flavonoids and hub targets. Immune-inflammatory dysregulation links obesity and IPF via NLRC4, SPI1, and NCF2. These genes serve as diagnostic biomarkers and therapeutic targets, with flavonoids showing intervention potential. Our findings advance mechanistic insights into obesity-related pulmonary fibrosis.
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