Inflammatory regulatory mechanisms and targeted therapy of antineutrophil cytoplasmic antibodies in atherosclerosis (Review).

Atherosclerosis is the core pathological basis of cardiocerebrovascular diseases, and inflammatory response runs through the course of its occurrence, progression, and adverse events. Antineutrophil cytoplasmic antibodies (ANCAs) are autoantibodies targeting the lysosomal components in the cytoplasm of neutrophils and monocytes, and their association with atherosclerosis and pathogenic effects have become a research hotspot in cardiovascular medicine. The present review systematically examined the core molecular mechanisms of ANCA‑mediated atherosclerosis, focusing on analyzing the pro‑atherogenic effects of ANCAs through the regulation of monocyte dysfunction, induction of the formation of neutrophil extracellular traps, and activation of the synergistic complement‑platelet pathway, and clarified the subtype‑specific pathogenic pathways mediated by myeloperoxidase‑ANCAs and proteinase 3‑ANCAs. The present review also summarized the clinical evidence linking ANCA positivity to the risk of atherosclerosis, plaque characteristics, and clinical outcomes and explores the precise intervention strategies for targeting ANCA‑related pathways in atherosclerosis. Finally, it highlighted the limitations of current research and future directions to provide a theoretical reference and novel insights for the risk stratification of populations at high risk of atherosclerosis and the precise management of residual inflammatory risk.