Identification of crucial disulfidptosis genes and regulatory biomarkers in diabetic retinopathy based on bioinformatics analysis

Diabetic retinopathy is characterized by retinal microvasculature dysfunction which remains a major cause of vision impairment. Recent findings indicate that disulfidptosis, a novel cell death mechanism, may play a role in DR pathogenesis, though its underlying mechanisms are not yet understood. Therefore, it is crucial to identify disulfidptosis-related biomarkers to advance the research on diabetic retinopathy. Transcriptome data from the GSE102485 and GSE160306 datasets were analysed to identify common differentially expressed genes. Weighted gene co-expression network analysis was applied to identify module genes associated with disulfidptosis in the GSE102485 dataset. Disulphidptosis-related differentially expressed genes were determined by overlapping common differentially expressed genes with key module genes. The MCC algorithm of the protein-protein interaction network was used to identify Five key biomarkers including ITGAM, C1QA, SPI1, TYROBP, and FCGR2B were identified with significant diagnostic potential for DR. Furthermore, immune infiltration and gene set enrichment analysis revealed their association with immune cell infiltration, particularly memory B cells and follicular helper T cells. Pathway enrichment analysis indicated roles in apoptosis and ribosome pathways, highlighting their potential in DR pathogenesis. Additionally, drug-target predictions identified Bevacizumab, Daclizumab, and Palivizumab as possible therapeutic options targeting C1QA and FCGR2B. These findings establish a theoretical foundation for leveraging disulfidptosis-related biomarkers in DR diagnosis and treatment.