PDF(Pubmed)
Abstract：
Neutrophils, which constitute the most abundant leukocytes in human blood, emerge as crucial players in the induction of endothelial cell death and the modulation of endothelial cell responses under both physiological and pathological conditions. The hallmark of preeclampsia is endothelial dysfunction induced by systemic inflammation, in which neutrophils, particularly through the formation of neutrophil extracellular traps (NETs), play a pivotal role in the development and perpetuation of endothelial dysfunction and the hypertensive state. Considering the potential of numerous pharmaceutical agents to attenuate NET formation (NETosis) in preeclampsia, a comprehensive assessment of the extensively studied candidates becomes imperative. This review aims to identify mechanisms associated with the induction and negative regulation of NETs in the context of preeclampsia. We discuss potential drugs to modulate NETosis, such as NF-κβ inhibitors, vitamin D, and aspirin, and their association with mutagenicity and genotoxicity. Strong evidence supports the notion that molecules involved in the activation of NETs could serve as promising targets for the treatment of preeclampsia.
摘要：
中性粒细胞,构成人体血液中最丰富的白细胞，在生理和病理条件下，在诱导内皮细胞死亡和调节内皮细胞反应方面发挥关键作用。先兆子痫的标志是全身性炎症引起的内皮功能障碍，其中中性粒细胞，特别是通过形成中性粒细胞胞外陷阱（NET），在内皮功能障碍和高血压状态的发展和延续中起关键作用。考虑到许多药物在先兆子痫中减弱NET形成（NETosis）的潜力，对广泛研究的候选人进行全面评估变得势在必行。这篇综述旨在确定在先兆子痫背景下与NETs的诱导和负调节相关的机制。我们讨论了调节NETosis的潜在药物，如NF-κβ抑制剂，维生素D,还有阿司匹林,以及它们与致突变性和遗传毒性的关系。强有力的证据支持这样的观点,即参与NETs活化的分子可以作为治疗先兆子痫的有希望的靶标。
