Glaucoma is a complex and progressive disease that primarily affects the optic nerve axons, leading to irreversible vision loss. Although the exact molecular mechanisms underlying glaucoma pathogenesis are not fully understood, it is believed that except increased intraocular pressure, a combination of genetic and environmental factors play a role in the development of the disease. Animal models have been widely used in the study of glaucoma, allowing researchers to better understand the underlying mechanisms of the disease and test potential treatments. Several molecular pathways have been implicated in the pathogenesis of glaucoma, including oxidative stress, inflammation, and excitotoxic-induced neurodegeneration. This review summarizes the most important knowledge about molecular mechanisms involved in the glaucoma development. Although much research has been done to better understand the molecular mechanisms underlying this disease, there is still much to be learned to develop effective treatments and prevent vision loss in those affected by glaucoma.

中文翻译：

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实验性青光眼模型中的分子途径

青光眼是一种复杂的进行性疾病，主要影响视神经轴突，导致不可逆的视力丧失。尽管青光眼发病机制的确切分子机制尚不完全清楚，但人们相信，除了眼压升高之外，遗传和环境因素的结合也在该疾病的发展中发挥着作用。动物模型已广泛用于青光眼研究，使研究人员能够更好地了解该疾病的潜在机制并测试潜在的治疗方法。青光眼的发病机制涉及多种分子途径，包括氧化应激、炎症和兴奋性毒性诱导的神经变性。这篇综述总结了有关青光眼发展的分子机制的最重要知识。尽管为了更好地了解这种疾病的分子机制已经进行了大量研究，但要开发有效的治疗方法并预防青光眼患者的视力丧失，仍有很多东西需要学习。