[1]雷婧艺,王卓灵,张茗茹,等.Notch信号通路在脓毒症血管内皮损伤中的作用机制研究进展[J].陕西医学杂志,2025,54(8):1145-1149.[doi:DOI:10.3969/j.issn.1000-7377.2025.08.027]
　LEI Jingyi,WANG Zhuoling,ZHANG Mingru,et al.Research progress on the mechanism of the Notch signaling pathway in sepsis-induced vascular endothelial injury[J].,2025,54(8):1145-1149.[doi:DOI:10.3969/j.issn.1000-7377.2025.08.027]
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Notch信号通路在脓毒症血管内皮损伤中的作用机制研究进展

《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
54
期数:
2025年8期
页码:
1145-1149
栏目:
综 述
出版日期:
2025-08-05

文章信息/Info

Title:
Research progress on the mechanism of the Notch signaling pathway in sepsis-induced vascular endothelial injury
作者:
雷婧艺1; 2; 王卓灵1; 张茗茹1; 韩继明1; 梁亮2
（1.延安大学医学院，陕西 延安 716000；2.空军军医大学基础医学院生物化学与分子生物学教研室 消化系肿瘤整合防治全国重点实验室，陕西 西安 710032）
Author(s):
LEI Jingyi 1; 2; WANG Zhuoling1; ZHANG Mingru1; HAN Jiming 1; LIANG Liang2
(1.Yan’an Medical College of Yan’an University,Yan’an 716000,China;2.Department of Biochemistry and Molecular Biology,School of Basic Medical Sciences,Air Force Medical University,State Key Laboratory of Holistic Integrative Management of Gastrointestina
关键词:
脓毒症; Notch信号通路; 血管内皮细胞; 内皮功能障碍; 靶向治疗
Keywords:
Sepsis; Notch signaling pathway; Vascular endothelial cells; Endothelial dysfunction; Targeted therapy
分类号:
R 631
DOI:
DOI:10.3969/j.issn.1000-7377.2025.08.027
文献标志码:
A
摘要:
脓毒症是由感染诱发的宿主反应失调导致的多器官功能障碍综合征，其发病率和致死率较高，其中血管内皮细胞（ECs）功能障碍被认为是脓毒症病理生理的核心环节。ECs通过屏障功能、凝血-纤溶平衡及免疫调节等机制维持微循环稳态，而脓毒症中病原体相关分子模式（PAMPs）与损伤相关分子模式（DAMPs）可激活ECs，引发糖萼降解、促炎表型转换及凝血紊乱，最终驱动器官衰竭。Notch信号通路作为调控ECs表型与功能的关键通路，通过调节ECs增殖、凋亡、紧密连接蛋白表达及炎症因子分泌，影响内皮屏障完整性。此外，Notch信号通路可加剧炎症级联反应及凝血失衡。研究发现，脓毒症患者血浆中可溶性Notch配体δ样蛋白1（sDLL1）显著升高，且Notch信号异常与内皮凋亡及微血栓形成密切相关。现对Notch信号通路在ECs表型与功能中的作用、在脓毒症血管内皮损伤中的作用机制及其作为脓毒症治疗靶点的潜在价值进行综述，以期为脓毒症精准诊断与靶向治疗提供理论依据。
Abstract:
Sepsis is a syndrome of multiple organ dysfunction caused by dysregulated host response to infection,with high incidence and mortality rates.Vascular endothelial cells (ECs) dysfunction is considered a core pathological element in sepsis.ECs maintain microcirculatory homeostasis through barrier function,coagulation-fibrinolysis balance and immune regulation.In sepsis,pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) can activate ECs,leading to glycocalyx degradation,pro-inflammatory phenotypic switching,and coagulation disorders,ultimately driving organ failure.The Notch signaling pathway,as a key regulator of endothelial cell phenotype and function,affects endothelial barrier integrity by modulating EC proliferation,apoptosis,tight junction protein expression and inflammatory cytokine secretion.Additionally,the Notch signaling pathway can exacerbate the inflammatory cascade and coagulation imbalance.Studies have found that plasma levels of soluble Notch ligand sDLL1 are significantly elevated in sepsis patients,and abnormal Notch signaling is closely related to endothelial apoptosis and microthrombus formation.This article reviews the role of the Notch signaling pathway in ECs phenotype and function,its mechanism of action in sepsis-induced vascular endothelial injury,and its potential value as a therapeutic target for sepsis,aiming to provide a theoretical basis for the precise diagnosis and targeted treatment of sepsis.

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备注/Memo

备注/Memo:
陕西省自然科学基础研究计划项目（2023-JC-YB-202）；消化系肿瘤整合防治全国重点实验室自主课题（2025GTEP007）
更新日期/Last Update: 2025-08-04