PCI术后支架内再狭窄是严重影响糖尿病心血管并发症患者预后的重要因素。血管内膜增生是支架内再狭窄的主要病理过程。但是以平滑肌细胞增殖为靶点的转化医学应用并未获得预期效果。近来有关研究提示内皮间质转化在促动脉粥样硬化形成中起着重要作用，但其在糖尿病支架内再狭窄形成中的作用及其机制尚不清楚。本课题组综合国内外研究现状并结合前期工作基础，提出脂肪细胞来源的exosomes（ADEs）通过其表面携带的Shh，激活内皮细胞Snail信号通路，促进内皮细胞间质转化，加速血管内膜增生，可能是支架内再狭窄关键环节的假说。本课题拟在临床、细胞、动物水平，应用基因工程、血管超声、流式细胞术、分子生物学等多种技术方法验证这一假说。该研究结果可为抑制糖尿病PCI术后支架内再狭窄、降低糖尿病心血管并发症死亡率提供新的思路和治疗靶点。

In-stent restenosis (ISR) has been demonstrated to be a key factor influencing the prognosis of diabetic cardiovascular complications. Intima hyperplasia was confirmed to play a vital role in promoting ISR. However, the translational medical research targeted on the proliferation of vascular smooth muscle cells has not completely achieved expected results. Recently, related researches showed that endothelial-mesenchymal transition (EndMT) might play an important role in the formation of atherosclerosis. But whether or not EndMT contributes to ISR and the underlying mechanisms remain unclear. According to current reports combined with our previous study, we hypothesize that adipocyte-derived exosomes (ADEs) might be the key point of ISR, which might induce EndMT and accelerate the process of intima hyperplasia by activating the Shh/Snail signaling pathway. In this study, we will verify this hypothesis in clinical study, cell experiments as well as animal experiments, taking advantage of the various techniques such as genetic engineering, vascular ultrasound examination, flow cytometry and molecular biological techniques, etc. Our study will provide new ideas and therapeutic targets on preventing ISR, which would be an effective pathway to decrease the mortality of diabetic cardiovascular disease.