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NLRP3 炎性小体在子痫前期中的作用。

Role of the NLRP3 Inflammasome in Preeclampsia.

机构信息

Department of Animal Science, Tokyo University of Agriculture, Atsugi, Japan.

Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.

出版信息

Front Endocrinol (Lausanne). 2020 Feb 25;11:80. doi: 10.3389/fendo.2020.00080. eCollection 2020.

DOI:10.3389/fendo.2020.00080
PMID:32161574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7053284/
Abstract

Reproduction involves tightly regulated series of events and the immune system is involved in an array of reproductive processes. Disruption of well-controlled immune functions leads to infertility, placental inflammation, and numerous pregnancy complications, including preeclampsia (PE). Inflammasomes are involved in the process of pathogen clearance and sterile inflammation. They are large multi-protein complexes that are located in the cytosol and play key roles in the production of the pivotal inflammatory cytokines, interleukin (IL)-1β and IL-18, and pyroptosis. The nucleotide-binding oligomerization domain, leucine-rich repeat-, and pyrin domain-containing 3 (NLRP3) inflammasome is a key mediator of sterile inflammation induced by various types of damage-associated molecular patterns (DAMPs). Recent evidence indicates that the NLRP3 inflammasome is involved in pregnancy dysfunction, including PE. Many DAMPs (uric acid, palmitic acid, high-mobility group box 1, advanced glycation end products, extracellular vesicles, cell-free DNA, and free fatty acids) are increased and associated with pregnancy complications, especially PE. This review focuses on the role of the NLRP3 inflammasome in the pathophysiology of PE.

摘要

生殖涉及一系列严格调控的事件,免疫系统参与多种生殖过程。免疫功能的失调会导致不孕、胎盘炎症和许多妊娠并发症,包括子痫前期 (PE)。炎症小体参与病原体清除和无菌性炎症的过程。它们是位于细胞质中的大型多蛋白复合物,在产生关键炎症细胞因子白细胞介素 (IL)-1β 和 IL-18 以及细胞焦亡方面发挥着关键作用。核苷酸结合寡聚化结构域、富含亮氨酸重复序列和pyrin 结构域包含 3(NLRP3)炎症小体是各种损伤相关分子模式(DAMPs)诱导的无菌性炎症的关键介质。最近的证据表明,NLRP3 炎症小体参与妊娠功能障碍,包括 PE。许多 DAMPs(尿酸、棕榈酸、高迁移率族蛋白框 1、晚期糖基化终产物、细胞外囊泡、无细胞 DNA 和游离脂肪酸)增加,并与妊娠并发症,特别是 PE 相关。这篇综述重点介绍了 NLRP3 炎症小体在 PE 病理生理学中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9111/7053284/5d80e028883d/fendo-11-00080-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9111/7053284/23a84446cd30/fendo-11-00080-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9111/7053284/5d80e028883d/fendo-11-00080-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9111/7053284/23a84446cd30/fendo-11-00080-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9111/7053284/5d80e028883d/fendo-11-00080-g0002.jpg

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本文引用的文献

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Inflammasomes: Their Role in Normal and Complicated Pregnancies.炎症小体:在正常和复杂妊娠中的作用。
J Immunol. 2019 Dec 1;203(11):2757-2769. doi: 10.4049/jimmunol.1900901.
2
Caffeic Acid Inhibits the Formation of Advanced Glycation End Products (AGEs) and Mitigates the AGEs-Induced Oxidative Stress and Inflammation Reaction in Human Umbilical Vein Endothelial Cells (HUVECs).没食子酸抑制晚期糖基化终产物(AGEs)的形成,并减轻AGEs 诱导的人脐静脉内皮细胞(HUVECs)氧化应激和炎症反应。
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Preeclamptic patient-derived circulating cell-free DNA activates the production of inflammatory cytokines via toll-like receptor 9 signalling in the human placenta.
尿酸与子痫前期:病理生理相互作用及炎性小体激活的新作用
Antioxidants (Basel). 2025 Jul 29;14(8):928. doi: 10.3390/antiox14080928.
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Increased platelet activation and thrombo-inflammation in early and late-onset preeclampsia.早发型和晚发型子痫前期中血小板活化增加及血栓炎症反应
Res Pract Thromb Haemost. 2025 Jun 24;9(5):102956. doi: 10.1016/j.rpth.2025.102956. eCollection 2025 Jul.
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Pyroptosis as a therapeutic target in preeclampsia: current research and future directions.细胞焦亡作为子痫前期的治疗靶点:当前研究与未来方向
Front Immunol. 2025 Jun 25;16:1622550. doi: 10.3389/fimmu.2025.1622550. eCollection 2025.
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Plasma Extracellular Vesicles from Preeclamptic Patients Trigger a Detrimental Crosstalk Between Glomerular Endothelial Cells and Podocytes Involving Endothelin-1.子痫前期患者的血浆细胞外囊泡引发肾小球内皮细胞和足细胞之间涉及内皮素-1的有害串扰。
Int J Mol Sci. 2025 May 22;26(11):4962. doi: 10.3390/ijms26114962.
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BNIP3-mediated mitophagy aggravates placental injury in preeclampsia via NLRP1 inflammasome.BNIP3介导的线粒体自噬通过NLRP1炎性小体加重子痫前期的胎盘损伤。
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Biochem Biophys Res Commun. 2019 Feb 5;509(2):624-631. doi: 10.1016/j.bbrc.2018.11.145. Epub 2018 Dec 31.
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