角膜上皮的稳定与完整依赖于角膜缘干细胞的增殖与分化，而角膜上皮干细胞缺乏可导致患者视力下降甚至失明。我们的近期研究表明，神经营养因子GDNF可能调控角膜缘干细胞Survivin/CRM1促进组织修复再生。本研究将分别从细胞、动物和疾病发生的角度评估GDNF、Survivin和CRM1维持和调控角膜上皮干细胞的增殖中的作用机制，分析并阐明正常及病变组织中GDNF、Survivin和CRM1的表达变化和特点及Wnt/β-catenin信号通路活化情况。尝试通过外源性GDNF体外治疗LSCD疾病有助于验证其可行性，并有望开发新的以Survivin/CRM1为靶点的滴眼液作为临床治疗产品。

Limbal stem cells, which reside in the corneal periphery, contribute to the homeostasis of the corneal epithelium. Any damage or disease affecting the function of these cells may result in limbal stem cell deficiency (LSCD). The condition may result in both severe pain and blindness. Despite the great successes of limbal epithelial transplantation, there still is room for improvement as overall success rate is 70% and visual acuity often remains suboptimal after successful transplantation. Our previous studies showed that glial cell line-derived neurotrophic factor GDNF may enhances limbal epithelial regeneration via changing the Survivin/CRM1 function. In this study, we will further investigate the key factors of GDNF/Survivin/CRM1 function in human limbal epithelia, and to uncover the potential therapy of GDNF to vastly improve the treatment of LSCD diseases. These findings will benefit fully understanding the mechanisms that limbal stem cells promote regeneration of human corneal epithelium by producing GDNF via a signaling pathway that activates Survivin/CRM1 and lead to a new therapeutic approach for treating limbal stem cell deficiency.