高血压心肌重构的发生发展与血管新生及炎症密切相关。AGGF1不仅具有重要的促血管生成作用，也是一种新的抗炎因子。我们前期实验发现，血管紧张素Ⅱ（AngⅡ）刺激野生（WT）小鼠2周后，给予AGGF1重组蛋白可显著增加心肌微血管密度，减少炎细胞浸润，减小心肌细胞面积，降低心肌细胞凋亡及纤维沉积，提示AGGF1可能通过促进血管新生，减轻炎症反应，抑制心肌肥大、心肌凋亡和纤维化，调节高血压心肌重构的发生发展。本课题拟通过给予AGGF1重组蛋白或中和抗体，在AngⅡ刺激体外培养的心肌微血管内皮细胞、心肌细胞以及AngⅡ诱导小鼠心肌重构模型中，阐明AGGF1对血管新生、炎症反应、心肌肥大、心肌凋亡及纤维化的作用，明确AGGF1参与心肌重构的信号通路的变化，从而为深入阐明高血压心肌重构的发病机制及寻找新的治疗靶点提供实验依据。

Recent findings have demonstrated that angiogenesis and inflammation are closely related to the occurrence and development of hypertensive cardiac remodeling. AGGF1 is an important angiogenic factor and novel anti-inflammatory factor. Our preliminary study found that WT mice were given Ang II about 2w, the microvascular density was significantly reduced, the inflammatory cells, the area of cardiomyocyte, the apoptosis and fiber deposition of myocardium were markedly increased as compared with sham control. The results were contrary after recombinant AGGF1 was given. Accordingly, we think AGGF1 possiblely regulate the development of myocardial remodeling by enhancing angiogenesis, inhibiting inflammation, hypertrophy, apoptosis and fibrosis of myocardium. In the present study, using the culture systems of cardiac microvascular endothelial cells and cardiomyocytes, using WT mice treated with Ang II and recombinant AGGF1 or AGGF1 neutralization antibody, we study the impact of AGGF1 on the myocardial angiogenesis, inflammation, hypertrophy, apoptosis and fibrosis, and clarify the pathological mechanism that the AGGF1 regulated the development of hypertensive cardiac remodeling, and suggest that it may be a potential target for the early prevention and treatment of hypertensive cardiac remodeling.