Abstract
BACKGROUND: Chronic 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. METHODS: First, 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). RESULTS: These 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. CONCLUSION: Our 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.