Neutrophil extracellular traps (NETs), composed of deoxyribonucleic acid (DNA), histones, and granule enzymes, exhibit a “double-edged sword” effect in retinal neovascularization (RNV) diseases. The formation of NETs involves classical lytic and non-lytic pathways, as well as peptidylarginine deiminase 4 (PAD4)-dependent and reactive oxygen species-dependent molecular mechanisms. Across different types of RNV, the roles of NETs vary markedly. In diabetic retinopathy, NETs accelerate disease progression by amplifying inflammatory responses, disrupting the blood-retinal barrier, and increasing vascular permeability. During specific stages of retinopathy of prematurity, NETs participate in the clearance of senescent vessels and promote beneficial vascular remodeling. In retinal vein occlusion, their pro-coagulant and pro-inflammatory properties may exacerbate thrombosis and ischemia. The functions of NETs are dynamically regulated by disease stage, microenvironmental factors, and interactions with immune cells. Therefore, therapeutic strategies aimed at clearing NETs (e.g., deoxyribonuclease I) or inhibiting NET formation (e.g., PAD4 inhibitors) may serve as complementary approaches to current anti-vascular endothelial growth factor therapies, although further studies are needed to elucidate optimal intervention timing, safety, and combination treatment strategies for clinical translation.