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连接炎症与静脉血栓形成:NLRP3炎性小体的联系

Bridging inflammation and venous thrombosis: the NLRP3 inflammasome connection.

作者信息

Wu Jian, Wang Zilong, Shao Wei, Mo Jianwen

机构信息

The First Clinical College, Gannan Medical University, Ganzhou, Jiangxi, China.

Ganzhou Key Laboratory of Osteoporosis Research, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.

出版信息

Front Cardiovasc Med. 2025 May 30;12:1584745. doi: 10.3389/fcvm.2025.1584745. eCollection 2025.

DOI:10.3389/fcvm.2025.1584745
PMID:40520933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12162639/
Abstract

NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome is a critical regulator of inflammatory responses in the body and is closely associated with the inflammatory processes of various diseases. In recent years, research has increasingly focused on the role of the NLRP3 inflammasome in venous thromboembolism (VTE). Venous thromboembolism is a common and potentially fatal vascular disease with a complex pathophysiology involving multiple cellular and molecular pathways. The NLRP3 inflammasome activates caspase-1 downstream, facilitating the maturation and secretion of pro-inflammatory cytokines such as IL-1β and IL-18, triggering local and systemic inflammatory responses. These inflammatory reactions can promote the recruitment and activation of immune cells (such as monocytes and neutrophils), platelet activation, endothelial cell damage, and aggregation, ultimately leading to thrombus formation. Additionally, the interaction of the NLRP3 inflammasome with the coagulation system further exacerbates the risk of thrombosis. In summary, the NLRP3 inflammasome plays a critical role in the development of venous thrombosis, and interventions targeting it may offer new insights and strategies for the prevention and treatment of venous thrombosis. This review provides an overview of the current understanding of how the NLRP3 inflammasome promotes venous thrombosis, highlighting recent preclinical research advancements and potential therapeutic agents in this field.

摘要

NLRP3(含NACHT、LRR和PYD结构域蛋白3)炎性小体是体内炎症反应的关键调节因子,与多种疾病的炎症过程密切相关。近年来,研究越来越关注NLRP3炎性小体在静脉血栓栓塞症(VTE)中的作用。静脉血栓栓塞症是一种常见且可能致命的血管疾病,其病理生理过程复杂,涉及多个细胞和分子途径。NLRP3炎性小体激活下游的半胱天冬酶-1,促进促炎细胞因子如IL-1β和IL-18的成熟和分泌,引发局部和全身炎症反应。这些炎症反应可促进免疫细胞(如单核细胞和中性粒细胞)的募集和激活、血小板活化、内皮细胞损伤和聚集,最终导致血栓形成。此外,NLRP3炎性小体与凝血系统的相互作用进一步加剧了血栓形成的风险。总之,NLRP3炎性小体在静脉血栓形成过程中起关键作用,针对它的干预措施可能为静脉血栓的预防和治疗提供新的见解和策略。本文综述了目前对NLRP3炎性小体如何促进静脉血栓形成的理解,重点介绍了该领域最近的临床前研究进展和潜在的治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/c8414a623c0a/fcvm-12-1584745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/db0b7332a4ce/fcvm-12-1584745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/814e5236cd7a/fcvm-12-1584745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/c8414a623c0a/fcvm-12-1584745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/db0b7332a4ce/fcvm-12-1584745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/814e5236cd7a/fcvm-12-1584745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d0/12162639/c8414a623c0a/fcvm-12-1584745-g003.jpg

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本文引用的文献

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Role of von Willebrand factor (VWF), platelets, and aberrant flow in the initiation of venous thrombosis.血管性血友病因子(VWF)、血小板及异常血流在静脉血栓形成起始过程中的作用
Sci Adv. 2025 Feb 7;11(6):eadr5250. doi: 10.1126/sciadv.adr5250. Epub 2025 Feb 5.
2
Palmitoylation-mediated NLRP3 inflammasome activation in teleosts highlights evolutionary divergence in immune regulation.棕榈酰化介导的硬骨鱼NLRP3炎性小体激活凸显了免疫调节中的进化差异。
Zool Res. 2025 Jan 18;46(1):3-14. doi: 10.24272/j.issn.2095-8137.2024.409.
3
Cellular and Molecular Mechanisms Leading to Air Travel-Induced Thrombosis.
导致航空旅行诱发血栓形成的细胞和分子机制。
Circ Res. 2025 Jan 3;136(1):115-134. doi: 10.1161/CIRCRESAHA.124.325208. Epub 2025 Jan 2.
4
Procoagulant platelet activation promotes venous thrombosis.促凝血血小板活化促进静脉血栓形成。
Blood. 2024 Dec 12;144(24):2546-2553. doi: 10.1182/blood.2024025476.
5
Neutrophil NLRP3 promotes cardiac injury following acute myocardial infarction through IL-1β production, VWF release and NET deposition in the myocardium.中性粒细胞 NLRP3 通过在心肌中产生 IL-1β、释放 VWF 和 NET 沉积来促进急性心肌梗死后的心脏损伤。
Sci Rep. 2024 Jun 24;14(1):14524. doi: 10.1038/s41598-024-64710-4.
6
Extracellular histones: a unifying mechanism driving platelet-dependent extracellular vesicle release and thrombus formation in COVID-19.细胞外组蛋白:驱动 COVID-19 中血小板依赖性细胞外囊泡释放和血栓形成的统一机制。
J Thromb Haemost. 2024 Sep;22(9):2514-2530. doi: 10.1016/j.jtha.2024.05.019. Epub 2024 May 28.
7
Intravenous high-dose anakinra drops venous thrombosis and acute coronary syndrome in severe and critical COVID-19 patients: a propensity score matched study.静脉注射大剂量阿那白滞素可降低重症和危重症 COVID-19 患者的静脉血栓栓塞和急性冠状动脉综合征风险:一项倾向评分匹配研究。
Sci Rep. 2024 May 29;14(1):12369. doi: 10.1038/s41598-024-62079-y.
8
Hot under the clot: venous thrombogenesis is an inflammatory process.热点凝块之下:静脉血栓形成是一个炎症过程。
Blood. 2024 Aug 1;144(5):477-489. doi: 10.1182/blood.2023022522.
9
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Hypertens Res. 2024 Jun;47(6):1654-1667. doi: 10.1038/s41440-024-01661-3. Epub 2024 Apr 11.
10
Platelet factor 4 promotes deep venous thrombosis by regulating the formation of neutrophil extracellular traps.血小板因子 4 通过调节中性粒细胞胞外诱捕网的形成促进深静脉血栓形成。
Thromb Res. 2024 May;237:52-63. doi: 10.1016/j.thromres.2024.03.005. Epub 2024 Mar 5.