The retina is susceptible to damage by oxidative stimuli due to its high oxygen consumption and long-term exposure to light radiation. Reactive oxidation arises from aging, infection, air pollution, smoking and reperfusion injury. Accumulation of photodamage, free radical damage, hemodynamic abnormalities, and ultimately oxidative damage to the RPE, therefore, damage caused by oxidative stimulation under the action of specific risk factors, such as genetic factors or environmental factors, can cause histopathological changes and even lead to disease. Studies have confirmed that hyper-oxidative stimulation does exist in patients with age-related macular degeneration (AMD). Moreover, it has been recently reported that oxidative stressor arsenite promotes the expression and transcription of VEGF mRNA, which also supports the important role of oxidative damage in CNV formation. AMD may be an immune-related chronic nonspecific inflammatory lesion. using immunohistochemistry, Patel et al. confirmed the presence of autoantibodies to retinal tissue in AMD eyes, with progressive staining of the inner nuclear layer of the vitreous wart group from early to advanced stages of AMD, suggesting that anti-retinal autoantibodies play an important role in the pathogenesis of AMD. C-reactive protein is a systemic inflammatory response Seddon et al. showed that elevated C-reactive protein levels are an independent risk factor for AMD.