<p>The pathogenesis of diabetic retinopathy DR is highly complex, and in recent years, increasing attention has been directed toward the role of the gut in its development. Evidence suggests that intestinal barrier dysfunction is a frequent pathological feature in both DR patients and animal models, facilitating the translocation of gut microbiota and their metabolites into the systemic circulation. On one hand, these translocated microbial components and metabolites activate intestinal immune cells, promoting the migration of gut-derived immune cells to the retina or choroid, thereby contributing to retinal neuroinflammation. On the other hand, they may compromise the integrity of the blood-retina barrier, disrupting the retinal microenvironment. This review explores the influence of the gut on DR pathogenesis through several key mechanisms: alterations in gut microbiota and their metabolites, impairment of intestinal barrier integrity, dysregulated gut immune responses, translocation routes of gut-derived components (including immune cells, microbes, and metabolites) to the retina, and the resulting retinal pathology and microglial-mediated neuroinflammation. By elucidating the pathological mechanisms underlying the gut-retina axis, we aim to identify critical molecular and cellular targets involved in DR progression and to provide new insights for the development of innovative therapeutic strategies.</p>