Atherosclerosis (AS) is a disease characterised by the accumulation of atherosclerotic plaques on the inner walls of blood vessels, resulting in their narrowing. In its early stages, atherosclerosis remains asymptomatic and undetectable by conventional pathological methods. However, as the disease progresses, it can lead to a series of cardiovascular diseases, which are a leading cause of mortality among middle-aged and elderly populations worldwide. Neutrophil extracellular traps (NETs) are composed of chromatin and granular proteins released by neutrophils. Upon activation by external stimuli, neutrophils undergo a series of reactions, resulting in the release of NETs and subsequent cell death, a process termed NETosis. Research has demonstrated that NETosis is a means by which neutrophils contribute to immune responses. However, studies on neutrophil extracellular traps have identified NETs as the primary cause of various inflammation-induced diseases, including cystic fibrosis, systemic lupus erythematosus, and rheumatoid arthritis. Consequently, the present review will concentrate on the impact of neutrophil extracellular traps on atherosclerosis formation, analysing it from a molecular biology perspective. This will involve a systematic dissection of their proteomic components and signal pathways.