Abstract
Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes and is the leading cause of blindness in young adults. Oxidative stress has been implicated as a critical cause of DR. Metabolic abnormalities induced by high-glucose levels are involved in the development of DR and appear to be influenced by oxidative stress. The imbalance between reactive oxygen species (ROS) production and the antioxidant defense system activates several oxidative stress-related mechanisms that promote the pathogenesis of DR. The damage caused by oxidative stress persists for a considerable time, even after the blood glucose concentration has returned to a normal level. Animal experiments have proved that the use of antioxidants is a beneficial therapeutic strategy for the treatment of DR, but more data are required from clinical trials. The aims of this review are to highlight the improvements to our understanding of the oxidative stress-related mechanisms underlying the development of DR and provide a summary of the main antioxidant therapy strategies used to treat the disease.
Highlights
Diabetes, a chronic metabolic disease, includes types I and II
The activity of Nox 2 increases in the retinas of diabetic mice. This increase is associated with increased production of reactive oxygen species (ROS) and the expression of intercellular adhesion molecule1 (ICAM-1) and vascular endothelial growth factor (VEGF), which can be inhibited by deletion of the Nox 2 gene [21]
Diabetic retinopathy (DR) is a leading cause of blindness in working-age adults, and oxidative stress plays an important role in its development
Summary
A chronic metabolic disease, includes types I (lack of insulin) and II (insulin resistance). Systemic inflammation caused by these metabolic alternations leads to hemodynamic changes, blood-retinal barrier (BRB) damage, the leakage of retinal microvessels and edema, a gradual thickening of the retinal vascular basement membrane, and a loss of pericytes. These lesions continue with the progression of diabetes. The nuclear factor, erythroid 2 like 2- (NFE2L2-) related pathway (NFE2L2 is known as Nrf2), GTP-binding proteins, and epigenetic modifications have attracted increasing attention in recent years [7,8,9] All these pathways are associated with the overproduction of ROS. We summarize several of the mechanisms induced by oxidative stress that cause DR and focus on the latest research into the treatment of the disease using antioxidants
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