肾素-血管紧张素-醛固酮系统在心血管疾病中的重要作用已得到广泛认可。基础研究和临床实践均表明，血管紧张素Ⅱ(AngⅡ)不是其唯一的活性物质。新近发现的肾素(前体)受体[(P)RR]及其病理生理作用备受关注。国外及我们的研究已证实(P)RR过度表达能够不依赖于AngⅡ的产生而激活细胞信号通路，介导细胞增殖和炎症反应，导致蛋白尿、心肌纤维化，引起高血压和血管舒张功能障碍。但受动物模型限制，(P)RR致动脉粥样硬化(AS)机制的在体研究尚为空白。微流控芯片技术的发明与应用，使细胞三维立体培养、模拟在体血管微环境成为可能。本研究拟应用微流控芯片的独特优势，观察不同切应力及高糖干预下，内皮细胞(P)RR表达的变化及其对G偶联蛋白、NF-κB 和对内皮细胞凋亡的影响。同时将单核细胞与内皮细胞在同一基质中共培养，观察(P)RR在单核细胞粘附、迁移改变中的作用，为AS防治提供新的靶点。

The importance of renin-angiotensin-aldosterone system in cardiovascular diseases is generally accepted. It was demonstrated that angiotensin II wasn’t the only active substrate by both experimental researches and clinical observations. Thus it was of great concern when (pro)renin receptor [(P)RR] was discovered in 2002. It was demonstrated that overexpression of (P)RR could activate cellular signal pathways, and increase cell migration, proliferation, and cause proteinuria, glomerular sclerosis, cardiac fibrosis, and result in hypertension and vascular diastolic dysfunction, independent of Angiotensin II. However, the atherogenic mechanism of (P)RR in vivo has not got yet for the limitation of animal model. It is of great help when the microfluidic chips was invented and applied to the biological field, which made it possible to 3D cell culture and imitation of microvascular environment in vivo. Our study aims to observe changes of (P)RR expression in endothelial cells and its effects on the key factor of cellular signal pathway, G-coupled protein, NF-κB and epithelial apoptosis, intervened by hyperglycemia and different shear stresses through microfluidic chips. Meanwhile, let monocytes roll over the epithelial cells cultured tunnels on chips to observe the effects of (P)RR in the adhesion and migration of monocyte. Try to detect a new target for the prevention and treatment of atherosclerosis.