Inflammatory regulatory mechanisms and targeted therapy of antineutrophil cytoplasmic antibodies in atherosclerosis (Review)
- 1Department of Clinical Laboratory, Bethune International Peace Hospital, Shijiazhuang, Hebei 050082, P.R. China
- 2Department of Clinical Laboratory, Baoding No. 1 Central Hospital, Baoding, Hebei 071000, P.R. China
- 3Teaching and Research Section of Human Body and Life, Non-Commissioned Officer School, Army Medical University, Shijiazhuang, Hebei 050081, P.R. China
Abstract
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.
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BibTeX
@article{cui2026inflammatory,
title = {{Inflammatory regulatory mechanisms and targeted therapy of antineutrophil cytoplasmic antibodies in atherosclerosis (Review)}},
author = {Jingjing Cui and Qi Cui and Jinying Dou and Xiaoyan Li and Wenlong Chang and Lanchun Shi and Liyun An},
journal = {International Journal of Molecular Medicine},
year = {2026},
month = oct,
doi = {10.3892/ijmm.2026.6023},
url = {https://doi.org/10.3892/ijmm.2026.6023},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Inflammatory regulatory mechanisms and targeted therapy of antineutrophil cytoplasmic antibodies in atherosclerosis (Review)
AU - Jingjing Cui
AU - Qi Cui
AU - Jinying Dou
AU - Xiaoyan Li
AU - Wenlong Chang
AU - Lanchun Shi
AU - Liyun An
PY - 2026
DA - 2026/10/22
JO - International Journal of Molecular Medicine
DO - 10.3892/ijmm.2026.6023
UR - https://doi.org/10.3892/ijmm.2026.6023
AB - 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.
SN - 1107-3756
SN - 1791-244X
ER -