Diabetes mellitus (DM) and its complications are an actual problem of modern medicine. This pathology continues to spread throughout the world like a non-infectious epidemic. In this review new data about the role of different cellular mechanisms in forming of diabetic retinopathy (DR), namely, oxidative-nitrosative stress, mitochondrial dysfunction, neurodegeneration and inflammation. A new approach to DR pathogenesis is the primacy of the neurodegenerative changes in the retina vs previously held views of the problem as а microvascular pathology of the eye only. At the moment, hyperglycemia is considered as the main etiological factor of DR. Activation of the oxidation of excess glucose triggers a cascade of reactions with the formation of oxidative and nitrosative stress. Mitochondria are the most sensitive to oxidative-nitrosative organelles in cells of the retina. Hyperglicemia-induced mitochondrial dysfunction, with cellular respiration disruption and increased production of free radicals in neurons of the retina, can promote their further degeneration and DR enhancing. Local inflammation in the retina, which is facilitated in DM, also considered as a new component of DR pathogenesis. In this case, the inflammatory cascade occurs at the molecular level without clinical manifestations of inflammation. The review provides analysis of modern literature data on this mechanism involving in retinal complications of DM. It is emphasized, that retinal inflammation in DM enhances neurodegeneration and promote retinopathy.