Retinal hypoxia and inflammation play important roles in the progression and outcome in retinal vein occlusion (RVO). Retinal hypoxia leads to the up-regulation of hypoxia-inducible factor-1α(HIF-1α), which promotes the expression of its downstream targets, such as VEGF, PLGF and the receptors, etc. Inflammatory cells mainly include retinal endogenous microglia and the exogenous leukocytes, especially the activated monocyte-macrophage, which are chemotactic and infiltrate in retina from the blood. Inflammatory factors including IL-1β, IL-6, IL-8, TNF-α and MCP-1 are produced and released in large quantities, and the inflammatory mediators are mainly produced from the disintegrated blood cells. A large number of inflammatory mediators, such as leukotrienes and prostaglandins, were produced from the cell membrane lipids under the action of phospholipase A2, lipoxygenase and cyclooxygenase. Under the combined action of retinal hypoxia and inflammation, a variety of pathological changes were observed in retina, such as the breakdown of the blood-retinal barrier, increased retinal vascular leakage, and macular edema, the appearance and expansion of non-perfusion areas, retinal neovascularization, the atrophy and thinness of inner retina, and so on. Therefore, early treatments with anti-VEGF and anti-inflammation therapies are of great importance for the treatment of macular edema secondary to RVO. (Int Rev Ophthalmol, 2022, 46: 173-178)