Diabetes causes various metabolic and physiological abnormalities in the retina, but the exact mechanisms contributing to diabetic retinopathy (DR) are unclear. Many molecular and physiological changes in the retina under diabetes are consistent with inflammation, and anti-inflammatory therapies have been found to inhibit DR development in animal models. This review discusses inflammatory mediators and their role in early and late DR, and explores the potential of anti-inflammatory approaches to prevent DR progression. In vivo studies are emphasized, with in vitro data used where relevant. Diabetic retinopathy is a vascular disorder characterized by two stages: nonproliferative (NPDR) and proliferative (PDR). Early stages involve retinal microaneurysms and capillary nonperfusion, while advanced stages include neovascularization and macular edema. Inflammation is increasingly recognized as a key factor in DR pathogenesis, with various inflammatory molecules, such as iNOS, COX-2, and VEGF, playing significant roles. Inflammatory processes contribute to retinal capillary degeneration, increased vascular permeability, and leukostasis. Inflammation in DR involves multiple pathways, including NF-κB activation, RAGE signaling, and cytokine production. Inflammatory molecules like TNF-α, IL-1β, and VEGF are elevated in DR, contributing to retinal damage. Anti-inflammatory therapies, such as COX-2 inhibitors, RAGE inhibitors, and TNF-α antagonists, have shown promise in reducing DR progression. However, current treatments have limitations, and further research is needed to identify effective anti-inflammatory targets. Inflammatory changes in specific cell types, such as endothelial cells, pericytes, and microglia, contribute to DR pathogenesis. Inflammatory mediators, including eicosanoids and lipid-derived molecules, play roles in vascular permeability and neovascularization. Therapies targeting these pathways, such as statins and salicylates, have shown potential in reducing DR progression. Anti-inflammatory drugs like aspirin and minocycline may help inhibit DR even in the presence of hyperglycemia. In summary, inflammation is a critical factor in the development and progression of diabetic retinopathy. Understanding the molecular mechanisms of inflammation in DR is essential for developing effective therapeutic strategies. Current research highlights the importance of targeting inflammatory pathways to prevent or treat DR.Diabetes causes various metabolic and physiological abnormalities in the retina, but the exact mechanisms contributing to diabetic retinopathy (DR) are unclear. Many molecular and physiological changes in the retina under diabetes are consistent with inflammation, and anti-inflammatory therapies have been found to inhibit DR development in animal models. This review discusses inflammatory mediators and their role in early and late DR, and explores the potential of anti-inflammatory approaches to prevent DR progression. In vivo studies are emphasized, with in vitro data used where relevant. Diabetic retinopathy is a vascular disorder characterized by two stages: nonproliferative (NPDR) and proliferative (PDR). Early stages involve retinal microaneurysms and capillary nonperfusion, while advanced stages include neovascularization and macular edema. Inflammation is increasingly recognized as a key factor in DR pathogenesis, with various inflammatory molecules, such as iNOS, COX-2, and VEGF, playing significant roles. Inflammatory processes contribute to retinal capillary degeneration, increased vascular permeability, and leukostasis. Inflammation in DR involves multiple pathways, including NF-κB activation, RAGE signaling, and cytokine production. Inflammatory molecules like TNF-α, IL-1β, and VEGF are elevated in DR, contributing to retinal damage. Anti-inflammatory therapies, such as COX-2 inhibitors, RAGE inhibitors, and TNF-α antagonists, have shown promise in reducing DR progression. However, current treatments have limitations, and further research is needed to identify effective anti-inflammatory targets. Inflammatory changes in specific cell types, such as endothelial cells, pericytes, and microglia, contribute to DR pathogenesis. Inflammatory mediators, including eicosanoids and lipid-derived molecules, play roles in vascular permeability and neovascularization. Therapies targeting these pathways, such as statins and salicylates, have shown potential in reducing DR progression. Anti-inflammatory drugs like aspirin and minocycline may help inhibit DR even in the presence of hyperglycemia. In summary, inflammation is a critical factor in the development and progression of diabetic retinopathy. Understanding the molecular mechanisms of inflammation in DR is essential for developing effective therapeutic strategies. Current research highlights the importance of targeting inflammatory pathways to prevent or treat DR.