肺血管内皮细胞屏障功能破坏是机械通气相关肺损伤（VALI）发生发展过程中最显著的病理改变，研究其发生机制对VALI的防治具有重要意义。微管蛋白在维持内皮屏障完整性中发挥着重要作用，我们的预实验结果发现机械通气过程中伴随着微管蛋白α-tubulin的乙酰化水平下降，为了探讨其具体调控机制，我们在小鼠模型中进行了转录组和蛋白组高通量测序，结合IPA数据库预测分析，提出假说：机械通气可以引起LncRNA-GM19897表达上调，继而其通过miRNA-1233-5p调控CXCR4的表达，CXCR4作为趋化因子受体，可以激活Rac1作用于微管蛋白系统，使α-tubulin乙酰化水平下降，最终致使内皮细胞通透性增加，出现以肺组织水肿和炎性细胞浸润为特征的肺损伤。本研究拟从分子、细胞和整体水平，用一系列研究方法，探讨VALI过程中内皮屏障功能破坏的具体机制，为揭示VALI的发生机制和防治措施提供新思路。

The damage of pulmonary vascular endothelial cell barrier function is the most significant pathological change during the development of mechanical ventilation-associated lung injury (VALI). It is important to study its mechanism for the prevention and treatment of VALI. Tubulin plays an important role in maintaining the integrity of endothelial barrier. Our preliminary results showed that the acetylation level of α-tubulin decreased during mechanical ventilation. In order to explore its specific regulatory mechanism, we conducted transcriptional and proteomic high-throughput sequencing in mouse models. Combined with IPA database prediction analysis, we proposed the hypothesis that mechanical ventilation can cause LncRNA-GM19897 up-regulates the expression of CXCR4 through microRNA-1233-5p. As a chemokine receptor, CXCR4 can activate Rac1 acting on tubulin system and decrease the level of α-tubulin acetylation, resulting in increased endothelial cell permeability and lung injury characterized by pulmonary edema and inflammatory cell infiltration. The purpose of this study is to explore the specific mechanism of endothelial barrier dysfunction in VALI by a series of research methods at the molecular, cellular and overall levels, and to provide new ideas for revealing the mechanism and prevention measures of VALI.