Last update:
14-Jan-2025

Diabetic retinopathy (DR) remains the leading cause of blindness in people with diabetes aged 40-70 years. The pathogenesis of DR is a real and still-unanswered question. The primary stages of disease onset concern the changes in the neural layers of the retina, which precede the vascular changes that currently define DR. This has led to a rise in interest in the cellular and molecular pathophysiology of the neurodegeneration associated with DR. Reactive oxygen species (ROS) are known to originate from photoreceptors. Additionally, increased levels of immature neurotrophic factors have also been implicated in the neuronal viability pathway. Moreover, the apoptotic pathways of retinal neurons and glial cells in the context of DR are also particularly important. Furthermore, in the context of DR, the apoptotic pathways of glial cells and retinal neurons are very significant. Therapeutic treatments may be possible if the caspases implicated and the molecular pathways involved in each cell type are clarified. At the cellular level, retinal glial cells are responsible for neuronal support and homeostasis; their disruption has been studied to be involved in DR neurodegeneration. Finally, retinal neurons cannot be completely separated from the vasculature. Further research into early neurodegeneration in DR provides the potential to find and target early changes in the retina of people with diabetes before detectable vascular changes.

Key words: Apoptosis, Diabetic retinopathy, Neurodegeneration, Oxidative stress, Retina.