局部低浓度将显著降低基质细胞衍生因子（SDF-1）促进梗死心脏修复的生物学功效，补充外源性SDF-1可以提高局部浓度、促进心脏修复，但现有方法存在较多局限。我们初步研究显示，与单纯的SDF-1相比，新型融合蛋白Annexin-V-SDF-1的补充更明显地改善了梗死心脏的功能，但确切机制尚不清楚。体外实验发现该融合蛋白可靶向性地结合凋亡细胞，同时保留SDF-1的生物学功效，鉴于凋亡细胞较长时间、广泛地存在于心肌梗死及周边区域，我们推测Annexin-V-SDF-1可靶向结合凋亡细胞，在梗死区域高浓度聚集，从而促进相关修复细胞归巢，加速血管新生和心肌再生等修复过程。本项目针对小鼠心肌梗死模型，进一步验证Annexin-V-SDF-1促进梗死心脏修复的高效性，并深入探讨该融合蛋白促进梗死心脏修复的机制，为全面阐明SDF-1的生物学功效和寻找修复梗死心脏的优化措施提供重要的理论依据和新的研究思路。

The beneficial effects of stromal cell-derived factor-1 (SDF-1), in terms of promoting myocardial repair, are limited by its low concentration in the infracted heart. Though supplementation of exogenous SDF-1 was shown to augment local SDF-1 concentration and facilitate myocardial repair, there are several important limitations with the current delivery approaches. We found in our previous study that a novel bioengineered fusion protein, Annexin-V-SDF-1, was associated with greater functional improvement of the infarcted heart in comparison with SDF-1. However, the underlying mechanism is to be studied. Our in-vitro experiments indicated that Annexin-V-SDF-1 acquired the ability of targeting apoptotic cells while retained the biological activity of SDF-1. Additionally, apoptotic cells are present at the infarct and border zone through the whole period of myocardial repair. Therefore, we hypothesize that Annexin-V-SDF-1 could specifically bind to apoptotic cells and accumulate in the infarcted heart, which in turn boost angiogenesis and cardiomyocyte regeneration via homing of stem cells. In current study, we aim at confirming the high efficiency of Annexin-V-SDF-1 in promoting myocardial repair and probing into the underlying mechanism. This will highlight theoretical basis for comprehensively understanding the biological effects of SDF-1, as well as provide a new approach to optimizing post-infarction myocardial repair.