肝窦内皮细胞在对乙酰氨基酚所致肝损伤中的作用及其机制

彭璐; 张琦; 祝欣欣; 曲爱娟; 王艳

doi:10.12449/JCH260836

肝窦内皮细胞在对乙酰氨基酚所致肝损伤中的作用及其机制

DOI: 10.12449/JCH260836

彭璐¹,
张琦²,
祝欣欣³,
曲爱娟²,
王艳^1, , ,

1.
北京大学第一医院感染疾病科，北京 100034
2.
首都医科大学基础医学院生理学与病理生理学系，北京 100069
3.
首都医科大学附属北京朝阳医院检验科，北京 100024

基金项目:

国家自然科学基金 (81870417);

国家自然科学基金 (82070605)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：彭璐负责文章撰写；张琦和祝欣欣负责资料收集整理；曲爱娟和王艳负责文章修改及定稿。

详细信息

通信作者:
王艳， wangyanwang@bjmu.edu.cn （ORCID： 0000-0002-8577-0527）

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出版历程
- 收稿日期: 2025-11-21
- 录用日期: 2026-01-21
- 出版日期: 2026-08-25

Role and mechanism of liver sinusoidal endothelial cells in acetaminophen-induced liver injury

Lu Peng¹,
Qi Zhang²,
Xinxin Zhu³,
Aijuan Qu²,
Yan Wang^{1
, ,
,}

1.
Department of Infectious Diseases，Peking University First Hospital，Beijing 100034，China
2.
Department of Physiology and Pathophysiology，School of Basic Medical Sciences，Capital Medical University，Beijing 100069，China
3.
Department of Clinical Laboratory，Beijing Chaoyang Hospital，Capital Medical University，Beijing 100024，China

Research funding:

National Natural Science Foundation of China (81870417);

National Natural Science Foundation of China (82070605)

More Information

Corresponding author: Wang Yan， wangyanwang@bjmu.edu.cn （ORCID： 0000-0002-8577-0527）

摘要

摘要: 对乙酰氨基酚过量所致肝损伤是急性肝衰竭的主要病因之一，其机制复杂。在此过程中，肝窦内皮细胞损伤是关键的早期环节，由氧化应激、细胞凋亡、纤溶/凝血系统失衡等因素共同介导。由此引发的肝窦内皮细胞功能障碍，会进一步造成肝窦微循环紊乱、炎症反应放大，并损害肝脏的再生修复能力，最终导致肝细胞坏死。本文旨在系统阐述肝窦内皮细胞在对乙酰氨基酚诱导肝损伤中的关键作用及其分子机制，以期为开发新的治疗策略与研究方向提供理论依据。
- 肝窦内皮细胞 /
- 醋氨酚 /
- 化学性与药物性肝损伤
Abstract: Liver injury due to acetaminophen overdose is one of the main causes of acute liver failure， with a complex pathogenesis. In this process， liver sinusoidal endothelial cell （LSEC） injury is a key early event jointly mediated by factors such as oxidative stress， cell apoptosis， and imbalance between fibrinolysis and coagulation. Subsequent LSEC dysfunction further induces sinusoidal microcirculatory disturbances， amplifies the inflammatory response， impairs the regeneration and repair abilities of the liver， and finally causes hepatocyte necrosis. This article systematically elaborates on the critical role and molecular mechanism of LSEC in acetaminophen-induced liver injury， in order to provide a theoretical basis for novel therapeutic strategies and research directions.
- Liver Sinusoidal Endothelial Cell /
- Acetaminophen /
- Chemical and Drug Induced Liver Injury

HTML全文

注： APAP，对乙酰氨基酚；NAPQI，N-乙酰基-P-苯醌亚胺；GSH，谷胱甘肽；TLR9，Toll样受体9；NLRP3，核苷酸结合寡聚结构域样受体家族热蛋白结构域相关蛋白3；saa1/2，血清淀粉样物质A1/2；TLR2，Toll样受体2；VCAM-1，血管细胞黏附分子1；PAR1，蛋白酶激活受体1；PAR4，蛋白酶激活受体4；ATP，腺苷三磷酸；LSEC，肝窦内皮细胞；VE-cadherin，钙黏蛋白；H₂O₂，过氧化氢，GTPase，鸟苷三磷酸酶；G12/13，鸟嘌呤核苷酸结合蛋白α12/13亚基；Gαq，鸟嘌呤核苷酸结合蛋白αq亚基。

图 1 APAP诱导LSEC损伤的机制

Figure 1. Mechanisms of APAP-induced LSEC injury

下载: 全尺寸图片幻灯片

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