自体静脉移植广泛应用于临床血管重建，但因为移植血管新生内膜增生，移植血管的远期通畅率仍有限。以往关于新生内膜增生狭窄的研究主要集中于血管内膜或中膜细胞。最近研究发现，移植血管外膜存在的干/祖细胞可参与血管壁内炎症微环境形成、促进新生内膜增生，但机制不详。我们以往研究表明乙醛脱氢酶2（ALDH2）对于维持缺血后微环境的动态平衡发挥重要作用，预实验又发现ALDH2能促进血管外膜干细胞（Sca-1+细胞）分化为平滑肌细胞，且ALDH2缺失能够减轻桥血管狭窄。由此我们推测：ALDH2通过促进处于炎性缺氧微环境中血管外膜干/祖细胞的分化增殖，进而加速移植静脉内膜增生性狭窄。为求验证，我们拟运用ALDH2基因敲除小鼠，从Sca-1+细胞、巨噬细胞交互作用等角度深入探究代谢模式及分化对微环境的影响。旨在明确ALDH2调控血管外膜干细胞等的分化和增殖导致桥血管狭窄的分子通路，为维持桥血管通畅提供有效靶点。

Autologous vein grafts remain the only surgical alternative for many types of vascular reconstruction, but the patency rate is still limited because of neointima formation within the grafted vessels. Previous work has mostly focused on the putative roles of cellular players that were derived from either the intima or media. In the recent studies, adventitial stem/progenitor cells have been proved to participate in neointimal formation in inflammatory microenvironment of vein grafts. After transplantation, the adventitial stem/progenitor cells of vein grafts are within ischemia, hypoxia and inflammatory microenvironment. However, the environmental regulatory mechanism is essentially unclear. Our previous data showed a vital role of aldehyde dehydrogenase-2 (ALDH2) in microenvironment homeostasis after ischemia. We have found that ALDH2 could enhance the differentiation of adventitial Sca-1+ cells to smooth muscle cells (SMCs) and ALDH2 deletion could ameliorate vein graft neointimal hyperplasia. Based on these previous findings, we hypothesized that ALDH2 promote vein graft neointimal hyperplasia via facilitating adventitial stem/progenitor cells differentiation surrounded by inflammatory and hypoxia microenvironment. To verify it, we will use ALDH2 knockout Sca-1+ cells，macrophages and mice to explore metabolic and differential characteristics of Sca-1+ cells and macrophages and associated reactive pathway molecules among them. This study focus on identifying the effects of ALDH2 on adventitial Sca-1+ cells differentiation and proliferation followed by vein graft neointimal hyperplasia. The findings might provide a novel therapeutic target for preserving vein graft patency.