心肌梗死后心肌炎症反应的适度发生是影响心脏重构的主要因素。过度炎症反应会导致不良心脏重构。这种炎症反应主要由缺血坏死的心肌细胞释放内源性危险信号激活Toll样受体（TLR）后产生，所以TLR信号活化调控在心梗后炎症反应的调控中发挥关键作用。寻找通过调控TLR信号活化而调控心梗后炎症反应及心脏重构的免疫分子具有重要的临床意义。我们前期研究显示丝/苏磷酸酶PPM1L能抑制TLR触发的炎性细胞因子产生，且预实验发现PPM1L表达水平在小鼠梗死心肌组织及急性心梗患者外周血PBMC中显著升高，提示PPM1L极可能通过作用于TLR活化来调控心梗后炎症反应。而蛋白磷酸酶在心梗后炎症损伤及心脏重构中的作用尚未见报道。在本项目中，我们拟利用PPM1L定点插入转基因小鼠构建心肌梗死模型，研究PPM1L在心梗后炎症反应及心脏重构中的作用和靶分子，并阐明其调控机制，为临床心梗后炎症损伤干预提供潜在治疗思路和靶点。

The inflammatory responses after myocardial infarction (MI) play important roles in the later cardiac remodeling. The excessive inflammatory responses will lead to adverse cardiac remodeling. Toll-like receptors (TLRs) recognize endogenous danger signals released by necrotic cardiomyocytes and trigger inflammatory responses. So, the control of TLR activation is very important for the magnitude and persistence of post-MI inflammation, however, the molecular mechanism underlying the regulation of post-MI inflammation through TLR signal pathway remain unclear. Our previous study showed that Ser/Thr phosphatase PPM1L significantly inhibited TLR-triggered inflammatory cytokine production, and in the preliminary experiment of this case, we further found that the expression of PPM1L markedly increased in the ischemic/infarcted myocardium of mice with MI. Additionally, the expression of PPM1L also significantly increased in the PBMCs of patients with acute myocardial infarction.Our results indicate that PPM1L may regulate post-MI inflammation through TLR signal pathway. However, there is no report that shows the role of protein phosphatase in post-MI inflammation and cardiac remodeling. In this case, we aim to investigate the role of PPM1L in post-MI inflammation and cardiac remodeling with PPM1L transgenetic mice as well as the underlying mechanisms, which will shed new light on the treatment of myocardial infarction.