血-气屏障结构功能失调被认为是ALI/ARDS发生的重要机制。肺泡II型上皮细胞诱导早期炎症反应和丧失修复受损肺泡结构是造成血-气屏障功能失调的重要原因，只有阐明肺泡II型细胞受损的机制才能阻止ALI/ARDS的发生发展。我们前期研究表明Alu RNA和肺泡II型上皮细胞焦亡均参与了ALI/ARDS进程，但Alu RNA和肺泡II型上皮细胞焦亡是否存在调控作用，以及这种调控作用是否为ALI/ARDS血-气屏障结构功能失调的主要机制尚不清楚。本课题首先拟从动物实验和细胞实验证实Alu RNA和肺泡II型上皮细胞焦亡与ALI/ARDS密切相关；其后进一步通过基因敲除动物实验证实Alu RNA调控肺泡II型上皮细胞焦亡是ALI/ARDS形成的关键；最后在细胞分子水平阐明Alu RNA在肺泡II型上皮细胞焦亡中调控的关键细胞内信号分子，为阻止ALI/ARDS的发生发展提供理论基础。

Dysfunction of blood-air barrier structure is considered to be an important mechanism of ALI/ARDS. Alveolar type II epithelial cells induce early inflammation and loss of repair of damaged alveolar structures is an important cause of blood-air barrier dysfunction. Only by elucidating the mechanism of alveolar type II cell damage can prevent the development of ALI/ARDS. Our previous research showed that both Alu RNA and pyrolysis of alveolar type II epithelial cell participate in the process of ALI/ARDS, but whether Alu RNA have a regulatory effect on alveolar type II epithelial cell pyrolysis and whether this regulatory effect is the main mechanism of structural dysfunction on blood-air barrier in ALI/ARDS is unclear. In this project, it is first proposed to verify from animal experiments and cell experiments that Alu RNA and alveolar type II epithelial cell pyrolysis are closely related to ALI/ARDS; after that, further gene knockout animal experiments confirmed that Alu RNA regulates alveolar type II epithelial cell pyrolysis is the key to the formation of ALI/ARDS; finally, at the cellular molecular level, it clarifies the key intracellular signaling molecules regulated by Alu RNA in the alveolar type II epithelial cell pyrolysis, which provides a theoretical basis for preventing the occurrence and development of ALI/ARDS.