2025/12/01 by Yue Gao, Yang Yang, Lu Xia +4
Medicine · #Chronic Obstructive Pulmonary Disease (COPD) Research #Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis #Neonatal Respiratory Health Research
paper · doi:10.1016/j.jfma.2025.12.034
openalex publication_date 2025/12/01 · openalex created_date 2025/12/23 · openalex updated_date 2026/07/22
BACKGROUND: Bronchopulmonary dysplasia (BPD) is a primary complication in preterm infants, involving multiple pathological processes. Current research indicates that lactylation may play a significant role in disease progression, but its specific mechanisms in BPD remain unclear. This study aims to explore the function of the lactylation signature in BPD. METHODS: We analyzed the GSE32472 dataset, which includes BPD and non-BPD infant samples, along with 335 lactylation-related genes (LRGs). Differentially expressed genes (DEGs) analysis was performed using the "limma" R package, followed by gene function analysis with "clusterProfiler". Weighted Gene Co-expression Network Analysis (WGCNA) and four machine learning methods were used to identify biomarkers, the "pROC" R package evaluated predictive performance, qPCR validated gene expression, CIBERSORT analyzed immune infiltration, and GSEA identified enriched pathways. RESULTS: WGCNA identified 15 BPD-related gene modules, with 46 lactylation-BPD genes intersecting with LRGs. Unsupervised clustering revealed two BPD subgroups with Cluster 1 enriched in immune regulation and Cluster 2 linked to apoptosis and inflammation. Six key genes (LDHB, PYGL, PFKFB2, KIF23, GK, CA4) showed high diagnostic potential (AUC >0.7), with LDHB significantly down-regulated in BPD. GSEA indicated these genes' involvement in T-cell activation and immune response pathways. CONCLUSION: This study revealed the lactylation signature in BPD and may enhance our understanding of BPD pathogenesis.