Retinopathy of Prematurity (ROP) is a blinding eye disease characterized by abnormal retinal vascular proliferation and is a major cause of visual impairment in children. Its pathogenesis is complex, involving multiple factors such as hyperoxia exposure, hypoxic compensation, oxidative stress, inflammatory responses, and abnormal angiogenesis, with oxidative stress playing a central role. It is characterized by excessive production of reactive oxygen species and impaired antioxidant function, leading to retinal vascular endothelial cell damage, formation of avascular areas, and abnormal vascular proliferation. Studies have shown that oxidative stress can promote the development and progression of ROP through vascular damage, nitrooxidative stress synergy, and interference with cellular metabolism. Current treatment strategies mainly include antioxidant agents (such as vitamin C, vitamin E, and lutein), signal pathway regulatory agents (such as nuclear factor erythroid 2-related factor 2 activators, signal transducer and activator of transcription 3 inhibitors), corticosteroids (such as Triamcinolone and Dexamethasone), and adrenergic receptor antagonists (such as Propranolol), but their efficacy and safety still require further validation. In the future, multidisciplinary collaboration should be strengthened to further explore the interactions between oxidative stress and other pathological mechanisms, and long-term follow-up studies should be conducted to develop safer and more effective strategies for the prevention and treatment of ROP, thereby improving the visual outcomes of preterm infants.