Fidarestat

Diabetic retinopathy (DR) is a significant microvascular complication of diabetes mellitus, projected to affect nearly 161 million individuals globally by 2045.This condition arises from chronic hyperglycemia leading to oxidative stress and inflammation, ultimately resulting in retinal damage and potential blindness.Aldose reductase (ALR2) is a critical enzyme involved in glucose metabolism through the polyol pathway, and its inhibition has emerged as a promising therapeutic strategy for preventing diabetic complications.This study aims to identify potential protein targets of ALR2 inhibitors and explore their mol. interactions through bioinformatics and docking studies, potentially guiding novel approaches for DR treatment.We utilized the Gene Expression Omnibus dataset GSE221521 to analyze differentially expressed genes (DEGs) between healthy individuals and DR patients, identifying 2,822 downregulated and 2,386 upregulated genes.Venn diagram analyses identified intersections between ALR2 inhibitor targets and DR-associated genes.Bioinformatics tools, including ClueGO for functional enrichment anal., highlighted significant signaling pathways such as the ECM-receptor interaction signaling pathway, the PPAR signaling pathway, and cholestrol metabolism pathways, elucidating their roles in DR pathogenesis.Furthermore, protein-protein interaction (PPI) network anal. identified ten hub genes MMP9, ESR1, CD36, FASN, FLNA, AGRN, CXCL10, EGR1, LRP5, and SIGLEC1 indicative of their critical roles in diabetic pathol.Mol. docking studies revealed that Zopolrestat exhibited the highest binding affinity toward key hub proteins, suggesting its potential efficacy in modulating diabetic retinopathy signaling pathways.Our findings indicate that ALR2 inhibitors may provide a therapeutic avenue for managing DR by targeting pivotal genes and pathways involved in its progression, thereby enhancing patient outcomes.