内皮细胞（EC）在血管内部空间和皮下组织之间形成半透性屏障。肺内皮屏障的完整性是通过涉及受体、信号分子、连接复合物和蛋白质调节的细胞骨架重组的协调细胞过程来维持的。在急性肺损伤（ALI）或更严重的急性呼吸窘迫综合征（ARDS）中，严重肺部炎症和/或感染引起的内皮功能障碍继发内皮屏障完整性丧失，导致肺水肿和低氧血症。促炎激动剂如组胺、凝血酶、缓激肽、白细胞介素1β、肿瘤坏死因子α、血管内皮生长因子、血管生成素2、血小板活化因子以及细菌毒素和活性氧，引起细胞骨架的动态变化结构、粘附连接解体以及血管内皮钙粘蛋白（VE-钙粘蛋白）从肌动蛋白细胞骨架上脱离，导致内皮通透性增加。内皮细胞与白细胞、血小板和凝血的相互作用增强了炎症反应。此外，感染过程中炎症浸润和相关促炎细胞因子的产生会导致 EC 死亡，从而进一步损害肺内皮屏障的结构完整性。尽管使用强效抗生素和积极的重症监护支持，ALI 的死亡率仍然很高，因为肺 EC 屏障破坏的机制尚未完全了解。在这篇综述中，我们总结了ALI和ARDS中内皮细胞骨架重组、内皮间连接、内皮炎症、EC死亡和内皮修复的最新研究进展，旨在为临床中潜在的诊断和治疗靶点提供一些线索。疾病的管理。

Endothelial cells (ECs) form a semi-permeable barrier between the interior space of blood vessels and the underlying tissues. Pulmonary endothelial barrier integrity is maintained through coordinated cellular processes involving receptors, signaling molecules, junctional complexes, and protein-regulated cytoskeletal reorganization. In acute lung injury (ALI) or its more severe form acute respiratory distress syndrome (ARDS), the loss of endothelial barrier integrity secondary to endothelial dysfunction caused by severe pulmonary inflammation and/or infection leads to pulmonary edema and hypoxemia. Pro-inflammatory agonists such as histamine, thrombin, bradykinin, interleukin 1β, tumor necrosis factor α, vascular endothelial growth factor, angiopoietin-2, and platelet-activating factor, as well as bacterial toxins and reactive oxygen species, cause dynamic changes in cytoskeletal structure, adherens junction disorganization, and detachment of vascular endothelial cadherin (VE-cadherin) from the actin cytoskeleton, leading to an increase in endothelial permeability. Endothelial interactions with leukocytes, platelets, and coagulation enhance the inflammatory response. Moreover, inflammatory infiltration and the associated generation of pro-inflammatory cytokines during infection cause EC death, resulting in further compromise of the structural integrity of lung endothelial barrier. Despite the use of potent antibiotics and aggressive intensive care support, the mortality of ALI is still high, because the mechanisms of pulmonary EC barrier disruption are not fully understood. In this review, we summarized recent advances in the studies of endothelial cytoskeletal reorganization, inter-endothelial junctions, endothelial inflammation, EC death, and endothelial repair in ALI and ARDS, intending to shed some light on the potential diagnostic and therapeutic targets in the clinical management of the disease.