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.