糖尿病视网膜病变（diabetic retinopathy, DR）是全球常见致盲性眼病,发病机制尚不清楚。最新研究表明，EphrinA1可以通过结合EphA2受体在病理性视网膜血管生成中发挥作用，然而其在DR新生血管形成中的作用未有研究。本项目以DR新生血管为研究对象，探讨以下四点问题：①探讨EphA2、EphrinA1及相关因子在DR大鼠视网膜的表达，寻找DR新生血管的分子基础；②探讨EphrinA1-EphA2 信号通路调控DR新生血管的分子机制；③在高糖诱导的血管内皮细胞中，通过改变EphA2的表达，测定MAPK通路分子的磷酸化水平，在细胞水平证实上述分子机制；④利用临床标本检测EphA2及其配体EphrinA1与DR血管生成的相关性。通过以上研究，将回答EphA2及其配体EphrinA1是如何调控DR新生血管生成这一科学问题，为DR的预防和治疗找到新的突破口。

Diabetic retinopathy (diabetic retinopathy, DR) is a common cause of blindness worldwide. The mechanism remains unclear. New research shows that EphrinA1 can bind to the EphA2 receptor play an important role in the pathologic retinal angiogenesis. The project in diabetic retinal neovascularization as the object of study, the EphA2 and its ligand EphrinA1 as the breakthrough point, to clarify the following four problems: Objective to explore the expression of EphA2 and its ligand EphrinA1, VEGF and related factors in the retina of DR rats, the molecular basis for DR neovascularization; By changing the EphA2 and its ligand EphrinA1 in vivo expression, discuss the key molecules in MAPK pathway phosphorylation effects, to elucidate the molecular mechanism of EphA2 and its ligand EphrinA1 regulation DR neovascularization; In cultured vascular endothelial cells, by changing the EphA2 and its ligand EphrinA1 expression, determination of MAPK pathway phosphorylation, confirm the molecular mechanisms at the cellular level; Correlation between polymorphism and DR EphA2 and its ligand EphrinA1 and related genes, revealing its role from a clinical perspective. Through the above researches, the answer of EphA2 and its ligand EphrinA1 is how to control this scientific problems DR neovascularization, may provide new therapeutic targets for the disease.