心肌梗死（MI）后局部炎症反应是心肌重塑和心力衰竭的重要发病机制。心脏干细胞研究提示其在心脏修复中发挥重要作用，成为医学前沿重点发展领域，然而对其干细胞类型以及作用机制尚不明确，亟待阐明。申请人利用Nestin-GFP转基因小鼠发现，Nestin+细胞为心脏间充质干细胞（CMSCs），移植于MI动物模型体内可以促进心功能修复，明显减少了疾病早期巨噬细胞的浸润及增加M2型巨噬细胞，且该细胞自身高表达巨噬细胞调节因子Periostin, 提示其可能参与MI后巨噬细胞炎症反应的调解。据此，本研究拟利用体内外模型、基因测序、基因干扰及Periostin基因敲除小鼠模型等方法，探讨Nestin+CMSCs的特性及调控巨噬细胞炎症反应的直接作用机制。通过上述研究，阐明Nestin+CMSCs在心肌修复中的作用机制，也为进一步明确适合移植的心脏干细胞类型，及进行MI细胞治疗提供新的思路和可靠的理论依据。

In myocardial infarction (MI), local inflammatory response is an important pathogenesis of myocardial remodeling and heart failure. Cardiac stem cells are reported to play an important role in cardiac repair, and becomes an advanced and promising field in the medical research. However, specific stem cell type and mechanism of cardiac repair in MI remains unclear. Our previous study have found that Nestin+ cells from heart of Nestin-GFP transgenic mice were resident cardiac mesenchymal stem cells (CMSCs). When transplanted in the animal model of MI, these Nestin+ cells promote the repair of cardiac function, significantly reduce macrophage infiltration in the onset of the disease and increase M2 type of macrophage. Moreover, Peirostin, a macrophage regulatory factor, was highly expressed in these cells.Taken together, these results suggests that Nestin+ CMSCs are involved in the macrophage-mediated inflammatory response after MI. Here, we explore the direct mechanism in which Nestin+ CMSCs modulate the inflammatory response of macrophages by in vitro and in vivo models, gene sequencing, gene interference and periostin knockout mice model. This study is the first to demonstrate that the mechanism of Nestin+ CMSCs in cardiac repair by targeting Periostin-mediated M2 macrophages recruitment, and also further clarifies the type of cardiac stem cells suitable for transplantation and provides a novel and reliable theoretical basis for cell therapy in MI.