中文摘要：

本文扼要报道青光眼和近视的病因、发病机理及干预研究的主要结果。通过对GZ.1、PN.1青光眼家系及散发性青光眼的研究,发现Myocilin基因的Pro370Leu突变,导致蛋白质错误折叠,内质网应激。我们提出了青光眼属于＂蛋白质构象病＂、＂线粒体病＂的学说,并研究了靶向siRNA术后抗疤痕、视神经保护药物、干细胞替代治疗及药物缓释系统在青光眼治疗中的应用,为实现青光眼＂分期靶点干预＂奠定了基础。在近视的研究中,从灵长类恒河猴自然动物模型的构建着手,着重研究光学离焦与近距离负荷对青少年近视发生发展的影响,并且深入探讨了近视的视网膜与中枢神经机制,同时提出了光学干预近视的新策略。这些围绕青光眼和近视基本问题进行的系列研究,将可能为其诊治提供新的模式。

英文摘要：

The paper briefly reports the preliminary research results, focusing on the pathogenesis, mechanisms and interference strategies of glaucoma and myopia. （1） The myocilin gene has been found a mutation in Pro370Leu in GZ.1 and PN.1 glaucoma pedigrees, and the theory of protein misfolding and mitochondria dysfunction in glaucoma was then firstly elucidated. We further explored the modulation of wound healing by siRNA, neuro-protection by targeting drugs with drug deliver system and stem cells / iPS in glaucoma therapy, which offer a revolutionary strategy for glaucoma： differential treatment for specific stages. （2） Natural myopia model was successfully established in rhesus monkeys and retinal mechanisms and central nervous system were both found to play an important role during myopia development, and a variety of new optical interventions were therefore employed on human beings by series of randomized, controlled, double-masked prospective clinical trials. All these preliminary results offer a new insight into the new model for the diagnosis and treatment of glaucoma and myopia.