The clinical role of miR-362-5p in diabetic retinopathy and its mechanism function in high glucose-induced human retinal microvascular endothelial cells

The identification of novel biomarkers holds promise for improving the diagnosis of diabetic retinopathy (DR). This study sought to evaluate the role of miR-362-5p in DR. Seventy patients with type 2 diabetes mellitus (DM) and 136 patients with DR were enrolled in this study. ROC curve analysis, logistic regression, and correlation analysis assessed the diagnostic potential and clinical associations of miR-362-5p in DR. A high glucose (HG)-induced human retinal microvascular endothelial cell (hRMEC) model was employed to evaluate the effect of miR-362-5p in DR through cell counting kit‑8, transwell assay, and enzyme‑linked immunosorbent assay. Bioinformatics analysis, dual‑luciferase reporter assay, and western blot (WB) assay were performed to validate the target interaction between miR-362-5p and CCND2. Compared with DM subjects, DR subjects showed upregulated miR-362-5p expression, which correlated with fasting blood glucose (mmol/L), 2-h oral glucose tolerance test (mmol/L), glycated hemoglobin (%), and best corrected visual acuity (logMAR), and served as a candidate diagnostic biomarker for DR. Further elevated miR-362-5p expression might also distingulish proliferative DR (PDR) from non-PDR (NPDR). In mechanism, CCND2 was identified as a downstream target. miR-362-5p inhibition attenuated HG‑facilitated cell proliferation, migration, inflammation (IL‑6, TNF‑α), and angiogenesis (VEGF, Ang‑2) in hRMECs through targeting CCND2. miR-362-5p upregulation correlated with DR severity, showed diagnostic potential for DR, and was associated with the progression of PDR. In vitro, inhibition of miR-362-5p attenuated HG-induced hRMEC injury by targeting CCND2, which might offer novel strategies for DR management.