Abstract: The core pathological feature of neovascular age-related macular degeneration (NVAMD) is the formation of choroidal neovascularization (CNV). The mechanisms underlying CNV formation are complex and not yet fully understood. Currently, vascular endothelial growth factor (VEGF) inhibitors are the first-line treatment for NVAMD and have achieved preliminary success. However, the inability of patients to benefit from long-term outcomes has become increasingly apparent. Recent studies have identified multiple critical immune factors that play significant roles in CNV formation. The recruitment and polarization of macrophages (M) are central to this process, with M2 polarization promoting CNV progression. Additionally, complement cascade activation, inflammasome activation, and the secretion of pro-inflammatory cytokines further drive macrophage recruitment and polarization, exacerbating CNV lesions. Based on these findings, combining complement inhibitors, anti-inflammatory cytokines, and macrophage polarization modulators with anti-VEGF therapy holds potential not only to slow or reverse CNV progression but also to reduce the occurrence of therapeutic resistance, offering new hope for NVAMD patients. (Int Rev Ophthalmol, 2025, 49:  38-44)

Key words: neovascular age-related macular degeneration, choroidal neovascularization, immune response