miR-106a-5p targets CREB1 to regulate the inflammatory response in diabetic retinopathy

Diabetic retinopathy (DR) is a leading cause of vision loss in diabetic patients, yet early diagnostic biomarkers and targeted therapies remain limited. While miR-106a-5p has been linked to inflammatory and metabolic regulation, its role in DR remains poorly characterized. This study mainly explores the diagnostic value and molecular mechanism of miR-106a-5p/CREB1 in DR. The relative expression of miR-106a-5p in 50 patients with diabetes only (NDR) and 60 patients with DR was detected by qRT-PCR. Construct a high glucose-induced ARPE-19 cell model to evaluate changes in cell proliferation, inflammatory factors such as TNF-α, IL-6, IL-1β, and CREB1 expression after transfection with miR-106a-5p mimetics. Dual luciferase validation of miR-106a-5p/CREB1 target. Clinical correlations were analyzed by Pearson and logistic regression. miR-106a-5p was significantly downregulated in DR compared to NDR (P < 0.0001), and the ROC curve indicated that miR-106a-5p had high accuracy in DR diagnosis (AUC = 0.85). It correlated inversely with FPG (r = − 0.77), HbA1c (r = − 0.68), and inflammatory markers (IL-6, TNF-α). Binary logic analysis identified miR-106a-5p as a risk factor for diabetic retinopathy (OR = 0.08, P < 0.001). In vitro, miR-106a-5p overexpression attenuated HG-induced inflammation by targeting CREB1 (P < 0.0001). miR-106a-5p is considered an innovative biomarker for the detection of DR, research is exploring the part of miR-106a-5p/CREB1 in regulating inflammation as well as affecting DR occurrence, providing new ideas for DR treatment.