临床试验显示骨髓干细胞移植治疗缺血性心肌病的疗效并不理想。探索合适的骨髓干细胞亚群及增强病人来源骨髓干细胞功效的干预措施，是提高骨髓干细胞临床疗效的迫切需求。血管紧张素II通过其AT1和AT2受体（AT2R）参与心肌损伤修复机制。对于AT2R介导的功能目前了解甚少。我们前期研究发现能向受损心肌选择性迁移并促进心肌修复的骨髓CD117+AT2R+干细胞亚群。本项目将深入探讨是否通过应用CD117+AT2R+干细胞亚群及激活AT2受体的干预措施能有效地增强病人来源骨髓干细胞治疗缺血性心肌病的疗效。研究内容包括系统分析缺血性心肌病人骨髓CD117+AT2R+（vs. CD117+AT2R-）细胞的自我更新，迁移及分化潜质和功能；通过小鼠（SCID）心梗模型体内评估验证应用病人骨髓CD117+AT2R+干细胞亚群结合激活AT2受体的干预措施改善心肌修复的有效性和临床可行性。

Clinical trials have shown that the therapeutic efficiency of autologous transplantation of bone marrow (BM) stem/progenitor cells for ischemic cardiomyopathy remains low. There is an urgent need in the clinical settings to enhance therapeutic potentials of autologous transplantation of stem/progenitor cells derived from patients with ischemic cardiomyopathy. Angiotensin II, interferes with cardiac repair mechanisms, via its AT1 and AT2 receptor (R). Little is known about AT2R-mediated cellular mechanisms in the heart. We have recently defined the BM CD117+AT2R+ cell population, which increases and mediates cardiac repair in response to acute myocardial infarction in rats. In this translational project, we hypothesize that the application of human BM CD117+AT2R+ cells in combination with preconditioning via AT2R activation may potentially offer new translational options to improve therapeutic efficiency of BM stem/progenitor cells derived from patients with ischemic cardiomyopathy. The main aims of the project are to characterize and explore the regenerative potentials of BM CD117+AT2R+ cells derived from patients with ischemic cardiopathy, and to further study their therapeutic efficiency upon modification via AT2R stimulation in myocardial infarction models of immunodeficient (SCID) mice (proof of concept).