介入和溶栓治疗使心肌梗死（MI）患者生存率得到很大提高。但MI继发的心肌纤维化重构及难治性心衰发生率逐年递增，成为医学领域亟需解决的热点问题。在MI缺血微环境刺激下，心肌细胞病理性死亡和间质成纤维细胞转分化激活是心肌纤维化重构的直接原因。寻找既能激发心肌内源性保护调控，又能改善缺血微环境刺激的关键分子，将成为纤维化防治不可或缺的干预靶点。E1A激活基因阻遏子（CREG）是成熟组织细胞中广泛表达的内稳态调控蛋白。本室研究证实，CREG在MI后心肌组织中低表达；减少CREG表达明显加重MI小鼠心肌纤维化重构，提示其参与了MI后心肌纤维化调控。亟此，本研究尝试将CREG作为MI后心肌纤维化重构的靶向分子，从其对抗巨噬细胞炎症、抑制心肌细胞损伤和成纤维细胞转分化3个调控角度入手，通过在体、组织学和细胞学研究深入阐明CREG保护MI后心肌纤维化重构的作用机制，以期为心肌纤维化防治提供新的研究思路。

After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus of motality post-MI myocardial remodeling and improve cardiac function. To explore the key molecule and the mechanism(s) that protects against the detrimental consequences of MI might be a potential targets for the treatment of post-MI myocardial remodeling.Cellular repressor of E1A-stimulated genes(CREG) is ubiquitously expressed in mature tissue and cells in mammals. The results from our laboratory demonstrated that CREG expressed at very low levels in myocardiac tissue after post-myocardiac infarction (MI). Moreover, reduction of CREG exaggerates the myocardial fibrosis after post MI. Taken together, CREG plays a critical role in modulation of myocardial fibrosis. The hypothesis we propose here is that CREG might involve in macrophage inflammation, myocardiac cell impair-recovery and myocardial fibroblasts phenotype transition. Our approach is to utilize a combination of established animal model with cardial fibrosis remodeling after post MI, tissue and cells models to delineate the mechanism by which CREG may confer its effects. The findings will highlight to provide an efficient pathway for the treatment of heart remodeling post MI.