The retina is one of the most metabolically active organs in the body. Although it is an extension of the brain, the metabolic needs of the retina and metabolic exchanges between the different cell types in the retina are not the same as that of the brain. Retinal photoreceptors convert most of the glucose into lactate via aerobic glycolysis which takes place in their cytosol, yet there are immense numbers of mitochondria in photoreceptors. The present article is a focused review of the metabolic dysregulation seen in retinopathies with underlying vascular abnormalities with aberrant mitochondrial metabolism and Hypoxia-inducible factor (HIF) dependent pathogenesis. Special emphasis has been paid to metabolic exchanges between different cell types in retinopathy of prematurity (ROP), age-related macular degeneration (AMD), and diabetic retinopathy (DR). Metabolic similarities between these proliferative retinopathies have been discussed.