如何调控自噬以修复脑I/R损伤，促进其后神经功能缺损修复和功能重建，是脑血管疾病康复研究重点之一。我们前期研究发现BMSCs外泌体（BMSCs-exos）可通过抑制mTOR及激活自噬，提高OGD/R细胞活性；同时，miR-144-3p靶向mTOR；过表达miR-144-3p可提高OGD/R细胞活性；BMSCs-exos能上调OGD/R细胞miR-144-3p水平。由此提出假说：BMSCs-exos通过miR-144-3p调控mTOR/TFEB自噬溶酶体通路，从而上调自噬以修复神经功能。本项目突破常规BMSCs移植后低存活率的瓶颈，以自噬为切入点，着重探索BMSCs-exos、miR-144-3p和mTOR/TFEB介导的自噬溶酶体通路在脑I/R损伤中的作用，通过设计体内外实验，采用基因敲除、慢病毒转染等技术，验证上述假说，为BMSCs-exos移植治疗脑I/R损伤的临床应用提供科学依据。

How to regulate autophagy to repair cerebral I/R injury and promote the repair and functional reconstruction of subsequent neurological defects is one of the focuses of cerebrovascular disease rehabilitation research. We previously found that BMSCs-exosomes (BMSCs-exos) can enhance the activity of OGD/R cells by inhibiting mTOR and activating autophagy. Meanwhile, miR-144-3p targeted mTOR. Overexpression of miR-144-3p increased the activity of OGD/R cells. BMSCs-exos up-regulated the level of miR-144-3p in OGD/R cells. It was hypothesized that BMSCs-exos regulate the mTOR/TFEB autophagy-lysosomal pathway through miR-144-3p, thereby upregulating autophagy to repair neural function. This project will break through the bottleneck of the conventional low survival rate after BMSCs transplantation, focus on autophagy to explore BMSCs-exos, miR-144-3p and mTOR/TFEB mediated autophagy-lysosomal pathway in the role of cerebral I/R injury, through the design experiments in vivo and in vitro, by using gene knockout, lentivirus transfection and other techniques, verify the above hypothesis, and provide a scientific basis for the clinical application of BMSCs-exos transplantation in the treatment of cerebral I/R injury.