1.复旦大学附属中山医院急诊科/复旦大学应急救援与急危重症研究所 上海 200032
2.武汉大学人民医院重症医学科 湖北 武汉 430060
袁莉,女,1994—,医学硕士,主要从事急性呼吸窘迫综合征的机制研究,E⁃mail:yuanlisolar@163.com
宋振举,男,1975—,医学博士,主任医师,主要从事脓毒症/急性肺损伤免疫调节研究,E⁃mail:song.zhenju@zs⁃hospital.sh.cn
收稿:2024-07-11,
纸质出版:2025-02-25
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袁莉,宋振举,王璐.急性呼吸窘迫综合征中肺血管内皮细胞损伤与修复的研究新进展[J].武汉大学学报(医学版),2025,46(02):212-219.
YUAN Li,SONG Zhenju,WANG Lu.Investigating pulmonary endothelial cell injury and repair: Exploring new intervention targets for acute respiratory distress syndrome[J].Medical Journal of Wuhan University,2025,46(02):212-219.
袁莉,宋振举,王璐.急性呼吸窘迫综合征中肺血管内皮细胞损伤与修复的研究新进展[J].武汉大学学报(医学版),2025,46(02):212-219. DOI: 10.14188/j.1671-8852.2024.0525.
YUAN Li,SONG Zhenju,WANG Lu.Investigating pulmonary endothelial cell injury and repair: Exploring new intervention targets for acute respiratory distress syndrome[J].Medical Journal of Wuhan University,2025,46(02):212-219. DOI: 10.14188/j.1671-8852.2024.0525.
急性呼吸窘迫综合征(ARDS)的发病率与死亡率持续居高不下,众多研究已经证实肺血管内皮细胞(EC)在ARDS的发病机制中扮演着至关重要的角色。肺血管内皮细胞是肺泡⁃毛细血管屏障的重要组成部分,参与气体交换、体液平衡和白细胞迁移等生理活动,当EC遭遇环境应激、感染性病原体或内源性危险信号时会被激活,从而由静息状态转变为促炎和促凝血的激活状态。过度激活的EC表现为炎症反应的失控、凝血活动的增强和内皮屏障的通透性增加,这可能导致弥散性血管内凝血、肺水肿和肺出血,进一步加重ARDS的病情。本文旨在阐述肺血管内皮细胞损伤以及肺血管内皮细胞再生和修复方面的最新研究进展,以期为寻找ARDS治疗的新靶点提供方向。
Acute respiratory distress syndrome (ARDS) remains a significant healthcare challenge
marked by high incidence and mortality rates. Emerging research underscores the critical role of pulmonary endothelial cells (ECs) in ARDS pathogenesis. The pulmonary endothelial cells are an important component of the alveolar⁃capillary barrier
involved in normal physiological activities such as gas exchange
fluid balance
and leukocyte migration. However
when confronted with environmental stressors
infectious agents
or internal danger signals
ECs undergo activation. This activation shifts them from a resting state to one that promotes inflammation and coagulation. If this activation becomes excessive
ECs can enter a state of dysfunction
marked by heightened inflammation
coagulation
and increased permeability. This can lead to disseminated intravascular coagulation
pulmonary edema
and pulmonary hemorrhage
all of which exacerbate ARDS progression. This comprehensive review seeks to shed light on the new targets of pulmonary endothelial cell injury and the modulation of pulmonary endothelial cells regeneration and repair. By exploring these aspects
the review aims to pave the way for the discovery of innovative therapeutic targets to combat ARDS.
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