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细胞外中性粒细胞诱捕网导致的内皮功能障碍在外周中性粒细胞诱捕网相关性疾病的发生和治疗中起重要作用。

Endothelial Dysfunction Induced by Extracellular Neutrophil Traps Plays Important Role in the Occurrence and Treatment of Extracellular Neutrophil Traps-Related Disease.

机构信息

Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Nanchang University, Nanchang 330006, China.

出版信息

Int J Mol Sci. 2022 May 17;23(10):5626. doi: 10.3390/ijms23105626.

DOI:10.3390/ijms23105626
PMID:35628437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9147606/
Abstract

Many articles have demonstrated that extracellular neutrophil traps (NETs) are often described as part of the antibacterial function. However, since the components of NETs are non-specific, excessive NETs usually cause inflammation and tissue damage. Endothelial dysfunction (ED) caused by NETs is the major focus of tissue damage, which is highly related to many inflammatory diseases. Therefore, this review summarizes the latest advances in the primary and secondary mechanisms between NETs and ED regarding inflammation as a mediator. Moreover, the detailed molecular mechanisms with emphasis on the disadvantages from NETs are elaborated: NETs can use its own enzymes, release particles as damage-associated molecular patterns (DAMPs) and activate the complement system to interact with endothelial cells (ECs), drive ECs damage and eventually aggravate inflammation. In view of the role of NETs-induced ED in different diseases, we also discussed possible molecular mechanisms and the treatments of NETs-related diseases.

摘要

许多文章已经表明,细胞外中性粒细胞诱捕网(NETs)通常被描述为其抗菌功能的一部分。然而,由于 NETs 的组成是非特异性的,过多的 NETs 通常会导致炎症和组织损伤。NETs 引起的内皮功能障碍(ED)是组织损伤的主要关注点,这与许多炎症性疾病密切相关。因此,本综述总结了 NETs 与 ED 之间在炎症作为介质的主要和次要机制方面的最新进展。此外,还详细阐述了强调 NETs 缺点的详细分子机制:NETs 可以利用自身的酶、释放颗粒作为损伤相关分子模式(DAMPs)并激活补体系统与内皮细胞(ECs)相互作用,导致 ECs 损伤,最终加重炎症。鉴于 NETs 诱导的 ED 在不同疾病中的作用,我们还讨论了 NETs 相关疾病的可能分子机制和治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/66b76adcb7ef/ijms-23-05626-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/e283cf8f1494/ijms-23-05626-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/2a4f55e99c7d/ijms-23-05626-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/566ff1e4dd3e/ijms-23-05626-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/66b76adcb7ef/ijms-23-05626-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/e283cf8f1494/ijms-23-05626-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/2a4f55e99c7d/ijms-23-05626-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/566ff1e4dd3e/ijms-23-05626-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b201/9147606/66b76adcb7ef/ijms-23-05626-g004.jpg

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