Comprehensive analysis of ferritinophagy-related genes and immune infiltration landscape in diabetic retinopathy

Background Diabetic retinopathy (DR) is deemed a microangiopathy and neurodegenerative disorder, which primary reason of visual impairment in the world. Ferritinophagy critical regulator ferroptosis has vital part etiopathogenesis DR. Nevertheless, its molecular mechanism DR remains to be expounded. Methods The GSE146615 dataset was adopted identify ferritinophagy-related differentially expressed genes (FRDEGs). interactions biological functions were described by means functional enrichment analysis (FEA). enriched gene sets analyzed utilizing set (GSEA) variation (GSVA). Identification hub performed protein–protein interaction (PPI) analysis. mRNA–miRNA, mRNA–transcription factors (TF), mRNA–drugs, mRNA–RNA-binding proteins (RBP) networks constructed. In addition, datasets GSE60436 GSE94019 utilized for validation. diagnostic performance FRDEGs assessed receiver-operating characteristic curve monofactor analysis, followed immune infiltration Lastly, quantitative real-time polymerase chain reaction (qRT-PCR) implemented analyze validation genes. Results total, identification eight completed differential expression FEA mainly implicated autophagy mitochondrion, mitochondrion disassembly, autophagosome assembly, organization pathways. GSEA GSVA interferon alpha response, ultraviolet response up, gamma apical junction, pical surface, allograft rejection BECN1 HERC2 displayed high accuracies sets. Immune revealed that several cells related ferritinophagy may play potential roles Finally, qRT-PCR validate upregulated as well downregulated BCAT2 ATG7 model. Conclusion BECN1, HERC2, ATG7, act biomarkers might regulate microenvironment influence development progression. This research can provide new insights into pathogenesis ferritinophagy.