角膜缘干细胞对于角膜上皮的损伤修复至关重要，持续性炎症会破坏角膜上皮正常的损伤修复能力。在皮肤等其他组织中的研究表明，炎症会引起干细胞衰老，导致损伤修复异常；而目前尚无角膜上皮干细胞衰老影响损伤修复的相关报道。我们前期研究发现：炎症因子可引起角膜上皮干细胞衰老标志p16INK4a表达上升，抑制STAT3的活化；p16INK4a缺失可以促进角膜损伤修复并活化STAT3，说明p16INK4a-STAT3通路可能通过调控角膜上皮干细胞衰老影响角膜的损伤修复。在此工作基础上，本课题拟通过角膜上皮干细胞、正常及p16INK4a缺失小鼠模型，深入研究p16INK4a-STAT3信号通路对于角膜上皮干细胞衰老的调控作用，阐明其对角膜上皮损伤修复的影响及作用机制，并通过对角膜上皮干细胞进行针对p16INK4a-STAT3通路的靶向干预，为临床促进角膜损伤修复提供新的理论依据和干预策略。

Corneal epithelial stem cells is very important for corneal epithelial wound healing, however chronic inflammation will impair the normal ability of corneal epithelial wound healing. The studies in other tissues such as skin suggest that inflammation may induce stem cell senescence and damage the wound healing, but there no similar reports in corneal epithelial wound healing. Our previous studies found that inflammatory factors can increase the expression of the marker of senescence p16INK4a and inhibit the activation of STAT3; the deficiency of p16INK4a can promote corneal wound healing and STAT3 activation, suggesting that p16INK4a-STAT3 pathway may affect the corneal wound healing by the regulation of senescence of corneal epithelial stem cell. So we want to deeply study the regulation effects of p16INK4a-STAT3 pathway on the senescence of corneal epithelial stem cell, and illustrate its effects and mechanism on corneal wound healing via the model of corneal epithelial stem cell, normal and p16INK4a knock out mouse. And we will further investigate the effects of target intervention of p16INK4a-STAT3 pathway in corneal epithelial stem cells on enhancing the ability of corneal epithelial wound healing. This study will enrich the knowledge and provide the novel targets for the promotion of corneal wound healing.