与ReVGMT相比,SeVGMT在体/离体提高重编程心脏纤维母细胞为心肌样细胞效率，改善MI心功能。迄今增强SeVGMT重编程心脏纤维母细胞的化合物鲜有报道。我们预实验结果提示：CTRP3、UCHL-1增强SeVGMT重编程心脏纤维母细胞；过/抑制表达心肌细胞CTRP3增加/减少心肌细胞UCHL-1的表达。为此，我们提出假说：CTRP3介导UCHL-1增强SeVGMT重编程心脏纤维母细胞保护MI心功能。为了验证这一假说，我们拟分离小鼠和人的心脏纤维母细胞，通过小鼠MI模型，采用FACS、病毒载体转染、RNA干扰等手段，从分子、细胞、组织以及动物整体水平等多方面探讨CTRP3对SeVGMT重编程心脏纤维母细胞作用，揭示CTRP3增强SeVGMT重编程CFs的信号通路及对MI心功能的保护机制。本研究将从CTRP3这个新视点为揭示MI心功能新的保护机制奠定基础，为MI心力衰竭的防治提供新的思路。

Sendai virus was more efficient than retroviral in reprogramming cardiac fibroblasts(CFs) into induced cardiomyocyte-like cells(iCMs ) with GMT in vitro and in vivo. Direct in vivo reprogramming with SeVGMT improves cardiac function after myocardial infarction. The signals present in vitro and vivo resulting in improved quality of reprogramming with SeVGMT remain unknown. Our previous studies showed C1q tumor necrosis factor related protein 3( CTRP3) and Ubiquitin C-terminal hydrolase-L1(UCHL-1) increase reprogramming cardiac CFs with SeVGMT.Overexpression of CTRP3 will increase expession of UCHL-1.Suppression of CTRP3 will decrease expession of UCHL-1. Thus, we speculated that CTRP3 may improve cardiac function after myocardial Infarction by increasing reprogramme of CFs with SeVGMT by mediating UCHL-1. We planed to isolate CFs of mice and human,construct MI model in mice, use FACS / vector transfection/ RNA interfering technology to reveal the role of CTRP3 in reprogramming CFs with SeVGMT and the mechanism of CTRP3 mediate UCHL-1 improving cardiac function after myocardial Infarction by increasing reprogramme of CFs with SeVGMT. Therefore, the present study may reveal the new mechanism of protecting of cardiac function after myocardial infarction and provide a new idea to prevent and cure cardiac insufficiency from a new perspective of CTRP3.