Abstract
Proliferative vitreoretinopathy (PVR) is a condition where abnormal cell growth in the retina can cause vision loss. Autophagy, a process that removes damaged cellular components, may play a role in PVR. Our research used bioinformatics analysis of gene expression data from PVR patients to identify differentially expressed genes (DEGs) and investigate their potential involvement in autophagy. We found a total of 3947 DEGs in the PVR, with 1296 upregulated and 2651 downregulated. Intersection with autophagy-related genes yielded 37 differential autophagy genes, which were used to construct a protein–protein interaction (PPI) network. Network analysis identified two hub genes, CASP3 and SQSTM1, with CASP3 showing strong correlation with multiple differential autophagy genes. Further analysis using the WGCNA co-expression algorithm revealed a pivotal module of 722 genes with strong correlation to PVR, which were enriched in 516 GO biological processes, 79 GO molecular functions, and 40 GO cellular components. Additionally, GSEA functional enrichment analysis showed that 56 pathways were enriched in CASP3 upregulated and downregulated groups, with the top 4 pathways significantly enriched in both groups. Our results indicated that autophagy and CASP3 may participate in the PVR pathogenesis and could be potential therapeutic targets for the treatment of this disease.
Published Version
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