Abstract: Retinitis pigmentosa (RP) is an inherited retinal disease. Non-genetic biological factors such as inflammation, autophagy and oxidative stress also play important roles in its pathogenesis and progression. Oxidative DNA damage is a key regulator of microglia activation and photoreceptor degeneration in RP and is also a mutation of endogenous antioxidant pathways including DNA repair, protection from oxidative stress, and genes associated with antioxidant defense (MUTYH, CERKL and GLO1 genes) activation. Exposure to oxidative stress alters the expression of microRNA and long noncoding RNA. Furthermore, upregulation of the P2X7 receptor causes macrophages and microglia to release pro-inflammatory cytokines and reactive oxygen species, leading to neuroinflammation and neurodegeneration in RP. Multi-pathway analysis suggests that oxidative microglia activation may trigger a vicious cycle of neuroinflammation and degeneration, suggesting that microglia may be a key therapeutic target for oxidative stress in RP.(Int Rev Ophthalmol, 2022, 46:  341-346)

Key words: retinitis pigmentosa, inflammation, oxidative stress, P2X7 receptor