ArticleAnimal models and experimental medicine2025
Identification of ferroptosis-related genes involved in chronic obstructive pulmonary disease based on bioinformatics analysis.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Unfolding Immune Dysregulation in COPD: Identification of a Three-Gene Signature and Functional Validation ofInternational journal of molecular sciences · 2026Article
- Identification and Functional Characterization of COPD Molecular Subtypes Based on Oxeiptosis-Related Genes via WGCNA and Machine Learning.International journal of chronic obstructive pulmonary disease · 2026Article
- Identification of ferroptosis-related genes involved in chronic obstructive pulmonary disease based on bioinformatics analysis.Animal models and experimental medicine · 2025Article
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6 authors.
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Abstract
backgroundChronic obstructive pulmonary disease (COPD) is a type of chronic respiratory disease. Studies confirmed that ferroptosis was involved in the progression of COPD, and its related mechanism is not clear. The aim of this study was to identify ferroptosis-related genes and reveal its pathological application in COPD.
methodsFirst, we downloaded two datasets from the Gene Expression Omnibus (GEO) to obtain the differential genes of COPD. Ferroptosis-related genes were obtained from the ferroptosis database, FerrDb. Next, we obtained the key genes in COPD rat to identify potential biomarkers using quantitative real-time polymerase chain reaction. Ferroptosis and inflammation were assessed using hematoxylin and eosin staining, lung function tests, and transmission electron microscopy (TEM).
resultsThese results were used to construct a COPD risk model with six key genes and explore the immunological characteristics of these genes. The resulting molecular subtype construction confirmed the importance of the key genes in COPD. Furthermore, we proved that ferroptosis occurred in the COPD rat model and identified the six key genes in rat lung tissue. TEM showed significant functional impairment and structural alterations in mitochondria, which is the key site of ferroptosis.
conclusionOur COPD risk model, incorporating six key genes, highlighted their immunological roles in COPD using bioinformatics analysis and in vivo experiments. We hope to provide the basis for the treatment targeting ferroptosis in COPD.
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