肺气血屏障受损是急性肺损伤（ALI）的主要病理改变，其中肺血管内皮细胞具有屏障和修复功能，其修复与疾病进展密切相关。近期研究发现，受损的内皮细胞可获得“干性”。我们前期研究显示CD146可能具有调控细胞干性转化的功能，且发现ALI小鼠肺组织中CD146 及其配体Galectins含量显著增加。提示：ALI受损的内皮细胞可通过CD146/Galectins调控内 皮细胞获得“干性”，但具体机制不明。本项目以CD146/Galectins通路为切入点，提出CD146/Galectins通过激活下游信号通路，调控内皮细胞获得“干性”，在肺内皮屏障修复中发挥关键作用。拟采用ALI动物及细胞模型，明确ALI中CD146/Galectins下游信号通路与内皮细胞“干性”获得的相关性，并进一步探讨内皮细胞受损后获得“干性”的具体调控机制，为ALI临床治 疗提供新靶点和思路。

The damage of the lung-blood barrier is the main pathological change of acute lung injury (ALI). Pulmonary vascular endothelial cells have barrier and repair function, and their repair is closely related to disease progression. Recent studies have found that damaged endothelial cells can gain "Stemness". Our previous studies showed that CD146 may have the function of regulating stemness transformation, and the content of CD146 and its ligand Galectins in lung tissue of ALI mice increased significantly. It is suggested that ALI-damaged endothelial cells may be regulated by CD146/ Galectins to obtain stemness, but the mechanism is still debatable. Utilizing CD146/Galectins as the innovation point, this project proposes that CD146/Galectins can play an important role in the repair of lung endothelial barrier by activating downstream signaling pathways and regulating endothelial cells to obtain "stemness". It is proposed to use ALI animal and cell model to determine the correlation between the downstream signaling pathway of CD146/Galectins in ALI and the "stemness" of endothelial cells. Furthermore, the specific regulatory mechanism of stemness of endothelial cells after injury is explored, which provides a new target and idea for clinical treatment of ALI.