Bioinformatics analysis implicates ferroptosis and key hub genes in the pathogenesis of endometriosis.

OBJECTIVE: Endometriosis (EMs) is a chronic gynaecological condition characterised by the ectopic growth of endometrial tissue; however, its molecular mechanisms remain insufficiently understood. Ferroptosis, an iron-dependent form of regulated cell death, has been suggested as a potential contributor to its pathogenesis. This study aimed to identify differentially expressed ferroptosis-related genes (DE-FRGs) in EMs through bioinformatics analysis and to explore their underlying molecular mechanisms. METHODS: The gene expression datasets GSE7305 and GSE25628 were obtained from the GEO database. Ferroptosis-related genes (FRGs) were extracted from the FerrDb database. DE-FRGs were identified by intersecting differentially expressed genes (DEGs) with FRGs across the two datasets. Protein-protein interaction (PPI) networks were constructed using STRING and Cytoscape software, while core genes were identified through the cytoHubba plugin. Functional enrichment analysis was performed via the KEGG pathway. RESULTS: A total of 11 DE-FRGs were identified, all of which demonstrated consistently upregulated expression in EMs tissues across both datasets. Four core genes - GATA6, KLF2, BGN and AEBP1 - were selected for further analysis owing to their significant enrichment. KEGG analysis indicated that these genes were particularly enriched in the 'taurine and hypo-taurine metabolism' and 'muscle cell cytoskeleton' pathways. CONCLUSION: This study identified GATA6, KLF2, BGN, and AEBP1 as potential core genes associated with ferroptosis in EMs, highlighting their roles in metabolic and cytoskeletal pathways. These findings provide a novel perspective on the pathogenesis of EMs and suggest new therapeutic targets that warrant further experimental validation.