Abstract
Diabetic mellitus-induced diabetic retinopathy is a significant cause of visual impairment and blindness in adults. Circular RNAs (circRNAs) have been shown to play initial roles in vascular progression. However, the mechanism underlying diabetes mellitus-induced vascular complications remains largely unknown. In circRNA chip experiments, circRSU1 was found to be generally overexpressed in diabetic retinopathy patients. Human retina endothelial cells were stably transfected with lentiviruses carrying a circRSU1 interference plasmid. CircRSU1 downregulation alleviated diabetes mellitus induced retina vascular dysfunction, resulting in decreased vascular endothelial growth factor levels, inflammatory responses and oxidative stress. Mechanistically, we showed that elevated circRSU1 expression upregulated the TAZ levels by sponging miR-345-3p. Downregulation of TAZ reversed the vascular dysfunction that was caused by increased circRSU1 expression under hyperglycaemic conditions. In conclusion, overexpression of circRSU1 promotes vascular dysfunction by sponging miR-345-3p to increase the TAZ levels under diabetic conditions. We provide evidence that circRSU1 is a potential therapeutic target for treating diabetes mellitus-induced vascular dysfunction.