移植静脉血管内皮细胞损伤和功能失调导致内膜增生是术后再狭窄的重要因素，尽快修复受损血管内皮细胞结构及其生物学功能即再内皮化是防治再狭窄的关键。内皮祖细胞(EPC)具有定向归巢、高效分化为血管内皮细胞的潜能，已广泛应用于受损内皮的修复。半乳糖凝集素1（GAL1）、神经菌毛素1（NRP1）均可表达于多种组织，具备免疫抑制功能，在胚胎神经系统、血管内皮系统发育、分化过程中起重要作用。在神经系统、肿瘤组织中GAL1-NRP1途径介导血管生成和受损血管修复。因此我们设想：在移植静脉适应动脉血流过程中，GALI-NRP1信号可能发挥与其在神经系统类似的功能，促进内膜修复，抑制桥血管内膜异常增生。本研究拟利用SaRNA,CRISPI-ON技术上调移植静脉内皮GAL1的表达，通过GAL1-NRP1信号募集EPC，发挥内膜保护功能，减轻移植静脉再狭窄。此研究将为预防移植静脉再狭窄提供临床可行的治疗策略。

Vascular intimal hyperplasia caused by vascular endothelial cell injury and dysfunction of autogenous vein graft are main factors of postoperative re-stenosis. The quick restoration of the structure and the biological function of damaged vascular endothelial cells, namely re-endothelialization, is crucial for the prevention of restenosis. Endothelial progenitor cells (EPC), which has a potency of orientated homing and differentiation as vascular endothelial cells, has been widely used for repair of damaged endothelium. Galectin-1 and Neuropilin-1 are involved in angiogenesis and re-endothelialization in nerve system and tumor tissues. We speculate that EPC can be attracted to the injured endothelial and promote re-endothelialization in the vein graft. SaRNA and CRISPR-ON technique will be applied to up-regulate GAL1 in vein graft, and the intimal protection will be recorded and the possible mechanism involved will be recorded. This finding will provide a new insight on the research of prevention of re-stenosis of autogenous vein graft, as well as a promising therapeutic target.