Original Data.

Proliferative diabetic retinopathy (PDR) is a microvascular complication of diabetes mellitus. Circular RNAs have been implicated in the pathogenesis of PDR. This study aimed to elucidate the specific mechanism by which circFTO contributes to PDR progression. circFTO expression was significantly upregulated in PDR patients and in high glucose (HG)-treated human retinal endothelial cells (HRECs). Knockdown of circFTO suppressed cell proliferation, migration, and tube formation in HG-treated HRECs. Furthermore, hsa-miR-141-3p levels were downregulated, while ZEB1 levels were upregulated in HG-treated HRECs. Dual-luciferase reporter assays demonstrated that hsa-miR-141-3p directly interacts with both circFTO and ZEB1. Additionally, hsa-miR-141-3p silencing reversed the effects of circFTO knockdown, and ZEB1 overexpression counteracted the effects of hsa-miR-141-3p mimic transfection. These findings suggest that circFTO promotes PDR progression via the hsa-miR-141-3p/ZEB1 axis. Collectively, our findings provide preliminary mechanistic insights into the role of circFTO in PDR progression, suggesting its potential as a candidate for further investigation as a diagnostic biomarker or therapeutic target.