Therefore, in the present study, a diabetic mouse model was established, and 661 w cells underwent high-glucose treatment to investigate the role of O-GlcNAc modification in the process of DR and to explore the effects of AMPK activation on this process and related mechanisms, with the aim of finding new therapeutic targets to delay the development of diabetic retinopathy. This evidence concerns the gene PRKAA1 and diabetic retinopathy.