间充质干细胞（MSC）能够促进急性呼吸窘迫综合征（ARDS）的修复，而其向损伤肺组织归巢率低限制其修复效果的提高。申请者在前期研究中发现ARDS时肺部水平升高的AngII主要通过MSC表面的AT2R促进黏着斑的形成增加进而促进MSC向损伤肺组织归巢。而近期研究发现NBR1受体介导的选择性自噬能够促进黏着斑的解离，从而抑制细胞迁移，并且AngII主要通过AT2R受体抑制自噬活动。因此，我们推测AngII-AT2R抑制NBR1介导的自噬，从而抑制黏着斑的解离，促进MSC的归巢。本研究拟体外明确AngII主要通过AT2R抑制自噬减少黏着斑的解离。进一步调控NBR1的表达，明确NBR1在AngII影响黏着斑解离中的作用。最后动物实验验证干扰MSC的NBR1受体能够促进MSC向损伤肺组织归巢，最终促进肺损伤的修复。本研究通过探讨AngII促进MSC归巢的机制，为优化MSC治疗ARDS提供新靶点。

Mesenchymal stem cell (MSC) could promote the repairation of acute respiratory distress syndrome (ARDS). However, the homing rate to injured lung tissue is low. In the previous study, we found that Ang II-AT2R promoted MSC migration primarily through focal adhesion formation. Interestingly, recent studies demonstrated that NBR1-mediated selective autophagy could affect focal adhesion formation and cell migration. What’s more, Ang II inhibits autophagy mainly through the AT2R receptor. Therefore, we speculate that Ang II-AT2R inhibits NBR1-mediated autophagy, thereby inhibiting the diasssembly of focal adhesions and promoting the homing of MSC. In this study, we try to make clear that Ang II promotes the diasssembly of focal adhesions mainly through AT2R-mediated autophagy. Furthermore, we regulate the expression of NBR1 to clarify the role of NBR1 in Ang II-induced focal adhesion dissociation. Finally, we try to use animal-level evidences to demonstrate that MSC downregulated with NBR1 receptor could promotes MSC homing to damaged lung tissue, ultimately contributing to the repairation of lung injury. In this study, we explore the mechanism by which Ang II promotes the homing of MSCs to injured lung and provide a new target for the optimization of MSCs for ARDS treatment.