早产儿视网膜病变(ROP)是婴幼儿首位致盲眼病，阻断病理性新生血管是治疗关键。但现有抗新生血管药物为“非选择性”，会影响早产儿视网膜正常血管发育。我们前期研究发现：颗粒素蛋白Scg3在ROP小鼠模型OIR的视网膜中高表达，并且Scg3抗体可“选择性”抑制视网膜的病理性新生血管，而不抑制组织的正常血管发育。因此我们推测：Scg3是 “高选择性”诱导ROP病理性新生血管的新型血管增殖因子，验证该假说并筛选Scg3特异性结合受体，将具备开发新型靶向抗新生血管药物和临床转化的重要潜力。因此，本研究拟通过体内外实验和噬菌体展示明确Scg3的血管增殖功能和“高选择性”特点，并通过基因敲除等技术进一步靶向验证，阐明其信号通路。在此基础上，拟通过体外实验、单细胞RNA测序等技术筛查Scg3特异性结合受体，探讨Scg3选择性高识别病理性血管的分子机制，可创新性为ROP甚至其他新生血管性疾病的防治提供新靶点。

Retinopathy of Prematurity（ROP） is a major cause of childhood blindness,.characterized with retinal pathological neovascularization (NV). The vasculature of retina and other organs in preterm infants are still developing. However, the current anti-NV agents are non-selective, which could inhibit not only pathological NV but also normal vasculature. Our preliminary study found that Secretogranin III（Scg3）was overexpressed in Oxygen induced retinopathy (OIR). The Scg3 monoclonal antibody could effectively reduce retinal neovascularization, and had no side effect on the development of retina, liver, and kidney, suggesting that Scg3 might induce pathological neovascularization selectively. Therefore, we speculated that Scg3 might be a novel selective angiogenic factor in OIR, which has the highest binding activity to pathological vessels and lowest binding activity to normal vessels. In the study, we aim at confirm the hypothesis that Scg3 could selectively regulate pathological neovascularization, understand the signaling pathway, and investigate the molecular mechanism of selective binding in further. It may provide an effective and safe therapeutic target for ROP.