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心肌缺血再灌注损伤中的中性粒细胞胞外陷阱形成:从机制到治疗(综述)

NETosis in myocardial ischemia-reperfusion injury: From mechanisms to therapies (Review).

作者信息

Zhang Ziyang, Wang Yanxin, Li Tie, Wang Hongfeng

机构信息

College of Acupuncture and Massage, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.

Department of Cardiovascular Medicine, The Third Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.

出版信息

Biomed Rep. 2025 May 13;23(1):113. doi: 10.3892/br.2025.1991. eCollection 2025 Jul.

DOI:10.3892/br.2025.1991
PMID:40420974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12105085/
Abstract

The present review describes the mechanisms of NETosis and its role in myocardial ischemia-reperfusion injury (MIRI), focusing on the release of neutrophil extracellular traps (NETs) by activated neutrophils. NETs, composed of depolymerized chromatin and granule proteins, are crucial for pathogen entrapment, infection control and immune regulation. However, NET formation, linked to neutrophil death (NETosis), exacerbates MIRI by promoting inflammation and tissue damage. To address therapeutic strategies for NETosis in MIRI, several potential clinically significant approaches were explored, including peptidylarginine deaminase 4 inhibition, DNase therapy, antioxidants, inflammation modulation, and antithrombotic treatments, which not only provide novel diagnostic biomarkers and therapeutic targets in MIRI, but are also expected to improve patient prognosis and advance the development of personalised medicine.

摘要

本综述描述了中性粒细胞胞外诱捕网形成的机制及其在心肌缺血再灌注损伤(MIRI)中的作用,重点关注活化中性粒细胞释放中性粒细胞胞外诱捕网(NETs)的情况。NETs由解聚的染色质和颗粒蛋白组成,对于捕获病原体、控制感染和免疫调节至关重要。然而,与中性粒细胞死亡(中性粒细胞胞外诱捕网形成)相关的NET形成通过促进炎症和组织损伤而加重MIRI。为了探讨针对MIRI中中性粒细胞胞外诱捕网形成的治疗策略,研究了几种具有潜在临床意义的方法,包括抑制肽基精氨酸脱氨酶4、DNA酶治疗、抗氧化剂、炎症调节和抗血栓治疗,这些方法不仅为MIRI提供了新的诊断生物标志物和治疗靶点,还有望改善患者预后并推动个性化医学的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ea/12105085/010cf14aab5a/br-23-01-01991-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ea/12105085/010cf14aab5a/br-23-01-01991-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ea/12105085/010cf14aab5a/br-23-01-01991-g00.jpg

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Cell Prolif. 2025 Feb 25:e70010. doi: 10.1111/cpr.70010.
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Stroke. 2025 Feb;56(2):527-532. doi: 10.1161/STROKEAHA.124.049961. Epub 2025 Jan 27.
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