Historically considered a metabolically inert cellular layer separating the blood from the underlying tissue, the endothelium is now recognized as a highly dynamic, metabolically active tissue that is critical to organ homeostasis. Under homeostatic conditions, lung endothelial cells (ECs) in healthy subjects are quiescent, promoting vasodilation, platelet disaggregation, and anti-inflammatory mechanisms. In contrast, lung ECs are essential contributors to the pathobiology of acute respiratory distress syndrome (ARDS), as the quiescent endothelium is rapidly and radically altered upon exposure to environmental stressors, infectious pathogens, or endogenous danger signals into an effective and formidable regulator of innate and adaptive immunity. These dramatic perturbations, produced in a tsunami of inflammatory cascade activation, result in paracellular gap formation between lung ECs, sustained lung edema, and multi-organ dysfunction that drives ARDS mortality. The astonishing plasticity of the lung endothelium in negotiating this inflammatory environment and efforts to therapeutically target the aberrant ARDS endothelium are examined in further detail in this review.

中文翻译：

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剃刀边缘：急性炎症性肺损伤/急性呼吸窘迫综合征的血管反应

历史上，内皮被认为是代谢惰性的细胞层，将血液与下面的组织分开，现在被认为是高度动态、代谢活跃的组织，对器官稳态至关重要。在稳态条件下，健康受试者的肺内皮细胞（EC）处于静止状态，促进血管舒张、血小板解聚和抗炎机制。相比之下，肺内皮细胞是急性呼吸窘迫综合征（ARDS）病理学的重要贡献者，因为静止的内皮细胞在暴露于环境压力源、传染性病原体或内源性危险信号时会迅速而彻底地改变，成为先天性的有效而强大的调节器。和适应性免疫。这些剧烈的扰动是在炎症级联激活的海啸中产生的，导致肺内皮细胞之间形成细胞旁间隙、持续的肺水肿和多器官功能障碍，从而导致 ARDS 死亡。本综述进一步详细研究了肺内皮在应对这种炎症环境中的惊人可塑性以及针对异常 ARDS 内皮的治疗努力。