Age-related macular degeneration (AMD) causes vision loss mainly due to apoptosis of retinal pigment epithelium cells and subsequent degeneration of photoreceptors.Active and passive smoking can increase the incidence of AMD and the progression risk of advanced AMD, and affect the treatment effect of wet AMD.Smoking can cause choroidal vasoconstriction, increased vascular resistance, vascular endothelial dysfunction, thinned choroid and ganglion cell complexes, resulting in impaired vascular reactivity of choroid and retinal vessels.Nicotine in cigarettes can lead to the overexpression of vascular endothelial growth factor (VEGF), which increases the permeability of vessel and proliferation of endothelial cells, thus induces the formation of choroidal neovascularization (CNV). Smoking can induce oxidative stress leading to oxidative damage, reduce the expression of complement factor H, increase the membrane attack complex, lead to macrophage dysfunction, promote the formation of drusen, and induce the formation of CNV.Therefore, a full and deep understanding of the relationship between smoking and CNV and AMD in controlling the occurrence of AMD and preventing the formation of CNV is of great significance for the early prevention of AMD and the exploration of more effective treatment approaches.