ALI/ARDS病死率仍居高不下，探索其机制意义重大。促进肺微血管损伤后屏障功能的恢复、降低肺微血管通透性，从而减轻肺水肿为目前研究热点。我们运用cre/loxp条件基因敲除技术成功构建在全身血管内皮细胞内敲除cdc42基因的小鼠模型，并发现敲除该基因后小鼠的胚胎发育滞后，血管稀少，胚胎水肿，无法发育成新生小鼠，提示cdc42可促进血管内皮细胞增殖并降低血管通透性。据此提出cdc42 在急性肺损伤后对肺微血管屏障功能的恢复具有促进作用的假说，并认为可能是通过促进内皮细胞分裂增殖和加强细胞间连接来发挥作用的。拟进一步利用cdc42基因敲除和cdc42过度表达的动物与细胞模型，从细胞分裂增殖和细胞间连接变化的角度入手研究cdc42对急性肺损伤后肺微血管屏障功能恢复的影响和作用机制，并明确相应的作用靶点和信号通路，为进一步干预其靶点和信号通路，减轻和治疗ALI/ARDS提供研究基础。

The case fatality of ALI/ARDS remains very high, it is very significant to research the mechanism of ALI/ARDS. Promoting the restoration of pulmonary microvascular barrier function and decreasing the permeability of pulmonary microvascular endothelial cells were the focus of research on ALI/ARDS. Utilizing the cre/loxp technology, we generated the endothelial specific cdc42-deleted mice model and found the deletion of cdc42 induced the delay of embryonic development, the less vasculature and the embryonic oedema, Which demonstrated that cdc42 could promote the growth and development of vascular endothelial cells and decrease the vascular permeability. Based on these result, we assumed that cdc42 could promote the restoration of lung microvascular barrier function through the promotion of the endothelial cellular proliferation and the strengthening of the cell-cell junction. Utilizing the cdc42 deficient and cdc42 overexpressed animal model and cellular model, we continued to research the effect of cdc42 on the restoration of pulmonary microvascular barrier function after ALI/ARDS and focused on the cellular proliferation and intercellular junction change, as well as the target protein and the signal pathway. This research could build the bases for continuing to interfere the target protein or signal pathway and treat the ALI/ARDS.