Ferroptosis related genes in retinopathy of prematurity: Screening for potential pharmacological targets

Purpose To elucidate the molecular mechanisms of retinopathy of prematurity (ROP) and identify potential drug targets for its treatment based on bioinformatics analysis. Methods We obtained gene expression profiles from data sets GSE123945 and GSE135844 in the Gene Expression Omnibus database. Differential expression analysis was performed on GSE135844 to identify differentially expressed genes (DEGs). Ferroptosis-related genes were retrieved from FerrDb, and Venn diagrams were used to identify overlapping genes between DEGs and ferroptosis-related genes. Functional enrichment analyses, including Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and gene set enrichment analysis, were conducted to explore the biological roles of these genes. Protein-protein interaction networks were constructed using the STRING database, and hub genes were identified using Cytoscape. Potential drug targets were screened using the Drug-Gene Interaction Database. Results We identified 23 DEGs associated with ferroptosis in ROP. These genes were significantly enriched in biological processes such as angiogenesis, vasculature development, and wound healing. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that the PI3K-Akt signaling pathway plays a central role in ROP pathogenesis. Gene set enrichment analysis identified the defense response as the most significantly enriched gene set. Hub genes, including HMOX1, ALB, and JUN, were identified through protein-protein interaction network analysis. Potential drugs targeting these hub genes, such as stannsoporfin, recombinant neurotrophic factors, zinc chloride, and irisolidone, were identified using the Drug-Gene Interaction Database. Conclusions Our study demonstrates the utility of bioinformatics approaches in identifying ferroptosis-related genes and potential drug targets for ROP. The findings provide a foundation for further experimental validation and the development of novel therapeutic strategies for ROP.