The mechanism of choroidal neovascularization (CNV) has not been fully investigated, and it is currently considered to be a multifactorial disease, the etiology of which is divided into ocular local and systemic factors. In terms of local ocular factors, CNV generation is a complex process involving multiple cytokines, and a relative or absolute increase in angiogenic factors caused by any cause can lead to neovascularization. The more accepted theory is the hypoxia theory. This theory suggests that tissue ischemia and hypoxia caused by abnormal blood circulation, oxidative damage and inflammatory response lead to the local release of various pro-angiogenic factors, and under the action of pro-angiogenic factors, the abnormally growing choroidal vessels break through Bruch’s membrane to enter the retinal pigment epithelium (RPE) or subepithelial growth of the nerve. Studies have confirmed that an imbalance between vascular growth factors and inhibitory factors plays an important initiating role in the formation of CNV, with vascular endothelial growth factor (VEGF) being the most potent angiogenesis-promoting factor identified to date. Systemic factors include hypertension, atherosclerosis, smoking and positive family history, while diet and UV light are suspected factors.