Abstract
AIMS: To investigate the role and underlying mechanisms of miR-4687-5p in diabetic retinopathy (DR) development. METHODS: A total of 180 DR patients were enrolled and stratified into non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) groups. Concurrently, 100 type 2 diabetes mellitus (T2DM) patients and 100 healthy volunteers were recruited as control groups. DR cellular models were established by treating ARPE-19 cells with high glucose (HG). Reverse transcription quantitative polymerase chain reaction was used to detect gene expression. An in vitro DR cell model was constructed to explore the potential mechanism of miR-4867-5p in DR. RESULTS: Serum miR-4687-5p expression was significantly elevated in DR patients compared to healthy controls and T2DM patients, with the highest levels observed in PDR patients. This miRNA exhibited excellent diagnostic value for DR. miR-4687-5p expression positively correlated with clinical parameters and pro-inflammatory cytokines in DR patients. In DR cell models, miR-4687-5p overexpression inhibited cell viability, promoted apoptosis, and exacerbated inflammatory responses, whereas miR-4687-5p knockdown exerted opposite effects. Mechanistically, miR-4687-5p contributes to DR progression by negatively regulating SIRT2 to modulate cell function and inflammation. CONCLUSIONS: miR-4687-5p is expected to become a biomarker for the early diagnosis of DR and a potential therapeutic target.