Retinitis pigmentosa (RP) is the most common form of inherited retinal dystrophy characterized by the progressive loss of vision. It is a rare disease. Despite being a genetic disease, its progression is influenced by oxidative damage and chemokines and cytokines released by the activated immune cells (e.g., macrophages or microglia). The role of oxidative stress is very important in the retina. Rods are the main consumers of oxygen (O2), so they are constantly exposed to oxidative stress and lipid peroxidation. According to the oxidative hypothesis, after rod death in the early stages of the disease, O2 would accumulate in large quantities in the retina, producing hyperoxia and favoring the accumulation of reactive oxygen species and reactive nitrogen species that would cause oxidative damage to lipids, proteins, and DNA, exacerbating the process of retinal degeneration. Evidence shows alterations in the antioxidant-oxidant state in patients and in animal models of RP. In recent years, therapeutic approaches aimed at reducing oxidative stress have emerged as useful therapies to slow down the progression of RP. We focus this review on oxidative stress and its relationship with the progression of RP.
Keywords: Antioxidant response; Cell death; Hyperoxia; Inflammation; Oxidative damage; Retinitis pigmentosa.
© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG.