Diabetic macular edema(DME)may occur at any stage of diabetic retinopathy(DR)and represents a significant cause of visual impairment in patients with DR. The pathogenesis of DME is complex, involving numerous risk factors. Recent studies have increasingly revealed that the occurrence and development of DME represents an intertwined pathophysiological process involving metabolic disorders, disruption of the blood-retinal barrier, amplified inflammatory responses, hemodynamic alterations, and the formation of hypoxic microenvironments. Multiple risk factors, including hyperglycaemia, dyslipidaemia, and genetic factors, synergistically drive this process. Risk factors and pathogenesis are a dynamic, interactive relationship in the progression of disease. Comprehensive management of risk factors such as blood glucose and blood lipids, along with multi-target interventions on core pathogenic mechanisms—such as combined anti-vascular endothelial growth factor(VEGF)and anti-inflammatory treatments, exploration of gene therapy and regulation of metabolic pathways—are expected to become key strategies for delaying the progression of DME.