中性粒细胞胞外诱捕网对动脉粥样硬化性心血管病的作用机制及其研究进展

doi:10.11958/20252054

天津医药 ›› 2025, Vol. 53 ›› Issue (10): 1104-1109.doi: 10.11958/20252054

中性粒细胞胞外诱捕网对动脉粥样硬化性心血管病的作用机制及其研究进展

金佳纯¹(), 陆彩霞¹^,², 吴燕君^3,△()

¹ 广东省职业病防治院（邮编 510300）
² 南方医科大学公共卫生学院
³ 深圳市光明区疾病预防控制中心

收稿日期:2025-05-26 修回日期:2025-07-10 出版日期:2025-10-15 发布日期:2025-10-12
作者简介:金佳纯（1982），女，副主任医师，主要从事职业健康检查和职业病诊断方面研究。E-mail：86521056@qq.com;^△审校者 E-mail:1158656959@qq.com
基金资助:
广东省基础与应用基础研究基金自然科学基金项目(2023A1515012756);广东省医学科研基金项目(B2025825)

The mechanism and research progress of neutrophil extracellular traps on arteriosclerotic cardiovascular disease

JIN Jiachun¹(), LU Caixia¹^,², WU Yanjun^3,△()

¹ Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China
² School of Public Health, Southern Medical University
³ Guangming District Center for Disease Cont and Prevention, Shenzhen

Received:2025-05-26 Revised:2025-07-10 Published:2025-10-15 Online:2025-10-12
About author:^△Reviser E-mail:1158656959@qq.com

金佳纯, 陆彩霞, 吴燕君. 中性粒细胞胞外诱捕网对动脉粥样硬化性心血管病的作用机制及其研究进展[J]. 天津医药, 2025, 53(10): 1104-1109.

JIN Jiachun, LU Caixia, WU Yanjun. The mechanism and research progress of neutrophil extracellular traps on arteriosclerotic cardiovascular disease[J]. Tianjin Medical Journal, 2025, 53(10): 1104-1109.

摘要/Abstract

摘要：

动脉粥样硬化性心血管病（ASCVD）是全球主要死亡原因之一，其进展与中性粒细胞胞外诱捕网（NETs）的病理作用密切相关。在动脉粥样硬化中，NETs通过促进炎症反应、诱导内皮功能障碍、促进血栓形成等机制，加剧病变进程。NETs释放的髓过氧化物酶（MPO）、中性粒细胞弹性蛋白酶（NE）及瓜氨酸化组蛋白H3（CitH3）等组分可激活免疫炎症级联反应，直接损伤血管内皮并促进血栓形成。在血管炎症中，NETs的形成受肌动蛋白调控，其释放的有害分子可诱导内皮细胞凋亡，通过氧化应激驱动炎症进展。NETs的降解与清除依赖于脱氧核糖核酸酶Ⅰ（DNaseⅠ）等酶的作用，其在动脉粥样硬化和血管炎症中的调节机制尚待深入研究。基于上述机制，NETs相关标志物展现出作为ASCVD新型诊断与预后评估生物标志物的潜力。该文旨在系统阐述NETs通过炎症激活、内皮损伤及血栓形成驱动ASCVD的核心病理机制，为靶向干预提供理论依据。

关键词: 动脉粥样硬化, 心血管疾病, 胞外诱捕网, 血管炎症

Abstract:

Atherosclerotic cardiovascular disease (ASCVD) is one of the leading causes of death worldwide, and its progression is closely related to the pathological effects of neutrophil extracellular traps (NETs). In atherosclerosis (AS), NETs aggravate the process of disease by promoting inflammatory response, inducing endothelial dysfunction, promoting thrombosis and other mechanisms. The components such as myeloperoxidase (MPO), neutrophil elastase (NE) and citrullinated histone H3 (CitH3) released by NETs can activate the immune inflammatory cascade, directly damage the vascular endothelium and promote thrombosis. In vascular inflammation, the formation of NETs is regulated by actin, and the released harmful molecules can induce endothelial cell apoptosis and drive the progress of inflammation through oxidative stress. The degradation and clearance of NETs depend on the action of enzymes such as deoxyribonuclease Ⅰ (DNase Ⅰ), and its regulatory mechanisms in atherosclerosis and vascular inflammation remain to be further studied. Based on the above mechanism, NETs-related markers have shown the potential as novel diagnostic and prognostic assessment biomarkers for ASCVD. This article aims to systematically elaborate the core pathological mechanism of NETs driving ASCVD through inflammatory activation, endothelial injury and thrombosis, providing a theoretical basis for targeted intervention.

Key words: atherosclerosis, cardiovascular diseases, extracellular traps, vascular inflammation

中图分类号:

R543.5，R323

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中性粒细胞胞外诱捕网对动脉粥样硬化性心血管病的作用机制及其研究进展

The mechanism and research progress of neutrophil extracellular traps on arteriosclerotic cardiovascular disease

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