Diabetic retinopathy (DR) is the most common microvascular complication of diabetes, seriously threatening the visual health of patients. Ceramide, as the core molecule of sphingolipid metabolism, abnormally accumulates in the retinal tissue of DR Patients and promotes the occurrence and development of DR By regulating pathological processes such as apoptosis, oxidative stress, inflammation and angiogenesis. Studies have shown that hyperglycemia can significantly alter the ceramide metabolic profile in the retina, leading to elevated levels and lipid toxicity. Moreover, there are regional changes in ceramide levels in the central area of the retina in DR Patients. Ceramides are involved in pathological processes such as retinal cell apoptosis, oxidative stress, mitochondrial dysfunction and blood-retinal barrier disruption, and shape the chronic inflammatory microenvironment of DR Through pro-inflammatory and immunomodulatory effects. In addition, sphingosine 1-phosphate regulates vascular development through its receptor and has a bidirectional interaction with vascular endothelial growth factor, participating in the formation of retinal neovascularization. In terms of treatment strategies, the lipid omics characteristics of tears and serum are expected to be used for non-invasive monitoring of DR, while intervention measures targeting neuramide include the use of synthetic inhibitors, metabolic balance regulation drugs, antibody neutralization, and novel delivery systems, etc. Although the clinical transformation process of the ceramide pathway to DR Is currently relatively lagging behind, in the future, it is necessary to move from "mechanism association" to "precise intervention", clarify its target specificity and elucidate its interaction with other pathways, in order to precisely enter the unmet clinical links such as metabolic disorders or neurodegeneration.