Oxidative stress in diabetic retinopathy

Abstract

Diabetic retinopathy (DR) is the leading cause of acquired blindness in working adults worldwide. Biochemical changes in DR contribute to both the microscopic structural and functional changes in the retina. All these alterations result in retinal damage that can be assessed by funduscopy, optical coherence tomography (OCT), and angioOCT. Reactive oxygen species (ROS) overproduction in the mitochondria is considered a causal link between elevated glucose and biochemical abnormalities in the pathophysiology of DR. Moreover, oxidative-induced pathways also seem to provide positive feedback to ROS production, resulting in a vicious cycle. ROS can directly damage lipids, proteins, and DNA, leading to cell death. To make the situation worse, antioxidant defenses are also impaired in diabetes. Otherwise ROS are involved in the production of inflammatory cytokines and growth factors such as interleukins or VEGF. Moreover, ROS not only contribute to the development of DR, but also play a role in its progression when the hyperglycemic insult is controlled. This phenomenon is called metabolic memory. Micro-RNAs, oxidative stress-related molecules, can be effective biomarkers for DR initiation and progression.