Lactate was originally thought to be a metabolic waste product of glycolysis produced by cells in hypoxic environment. In recent years, increasing evidence has indicated that lactate plays a crucial role in the physiological and pathological processes of the retina. Lactate is transported via monocarboxylate transporters in different retinal cell types such as photoreceptor cells and Müller cells to maintain the high metabolic demand of the retina. In addition to serving as oxiditive substrate for energy, lactate can mediate intracellular signal transduction through receptor G protein-coupled receptor 81, participating in the maintenance of retinal homeostasis and the progression of pathological neovascularization. Moreover, lactate-mediated protein lactylation directly regulates gene expression in microglia and T lymphocytes, which has gradually become a new hotspot in the field of retinal pathological neovascularization and neuroinflammation. Therefore, the regulation of lactate metabolism may provide novel perspectives for the treatment of retinal lactic acid metabolism disorders such as age-related macular degeneration and retinitis pigmentosa.