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Oxidative stress in retinal cells refers to an imbalance between the production of reactive oxygen species (ROS) and the capacity of antioxidant defenses within the retina. This state leads to cellular damage through modification of proteins, lipids, and DNA. It plays a central role in the pathogenesis and progression of several major retinal diseases including age-related macular degeneration, glaucoma, diabetic retinopathy, and retinal vein occlusion. Excessive oxidative stress can induce apoptosis in key cell types such as retinal pigment epithelial cells and ganglion cells. Therapeutic strategies targeting oxidative pathways—such as free radical scavengers like edaravone—have shown promise by reducing cell death and tissue damage through inhibition of pro-apoptotic signaling cascades like JNK and p38 MAPK pathways. However, "oxidative stress" itself is not a discrete molecular target but rather a pathological process involving multiple molecules and pathways.
Free radical scavenging to reduce reactive oxygen species and prevent oxidative damage
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