Ongoing efforts are oriented towards the development of novel therapeutic agents to repress lung hyperpermeability responses due to inflammation. The endothelial barrier dysfunction triggered by such events, may eventually lead to severe cardiovascular complications, such as the Acute Respiratory Distress Syndrome. Hsp90 inhibitors are anticancer compounds, associated with strong anti-inflammatory responses in the endothelium. Our latest observations in experimental models of Acute Lung Injury suggest that P53 orchestrates, at least in part, such activities. Remarkably, both Hsp90 inhibition and P53 induction are associated with the activation of the Unfolded Protein Response element. The purpose of the current manuscript, is to introduce the hypotheses that UPR induction protects the vasculature against inflammation.

中文翻译：

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展开的蛋白质反应支持内皮屏障功能。

正在进行的努力是针对新型治疗剂的开发，以抑制由于炎症引起的肺通透性过高的反应。由此类事件触发的内皮屏障功能障碍可能最终导致严重的心血管并发症，例如急性呼吸窘迫综合征。Hsp90抑制剂是抗癌化合物，与内皮中的强烈抗炎反应有关。我们在急性肺损伤实验模型中的最新观察结果表明，P53至少部分编排了此类活动。值得注意的是，Hsp90抑制和P53诱导均与未折叠蛋白反应元件的激活有关。当前手稿的目的是介绍关于UPR诱导保护脉管系统免受炎症影响的假设。