Abstract：
Glaucoma is a progressive optic neuropathy characterised by retinal ganglion cell degeneration and visual field loss. Glaucoma is considered to be the leading cause of blindness in the industrialised countries. Oxidative damage is an important pathogenic factor in glaucoma, which triggers trabecular meshwork (TM) degeneration, which then leads to intraocular hypertension. Neurodegenerative insults during glaucomatous neurodegeneration initiate an immune response to restore tissue homeostasis. However, the oxidative stress (OS) that develops during the pathogenic processes of glaucoma, along with the agerelated OS, plays a critical role in shifting the physiological equilibrium. In the TM from glaucoma donors, proinflammatory markers were found, which were induced by the activation of a stress response. Chronic changes in the composition of antioxidants found in aqueous humour may induce alterations in TM as well as in the optic nerve head cells. Highlighting the pathogenic role of reactive oxygen species (ROS) in glaucoma has implications in preventing this disease. Various clinical trials are available to test the efficacy of antioxidant drugs in glaucoma management. In this review, we discuss the OS as a therapeutic target, suggesting that the modulation of a pro-oxidant/antioxidant status might be a relevant target for glaucoma prevention and therapy.
摘要：
青光眼是以视网膜神经节细胞变性和视野丧失为特征的进行性视神经病变。在工业化国家，青光眼被认为是导致失明的主要原因。氧化损伤是青光眼的重要致病因子,引发小梁网(TM)变性，然后导致高眼压。青光眼神经变性过程中的神经变性损伤引发免疫反应以恢复组织稳态。然而,在青光眼致病过程中产生的氧化应激（OS），以及相关的操作系统，在改变生理平衡中起着至关重要的作用。在青光眼捐赠者的TM中，发现了促炎标志物，是由应激反应的激活引起的。在房水中发现的抗氧化剂组成的慢性变化可能会引起TM和视神经头部细胞的变化。强调活性氧（ROS）在青光眼中的致病作用对预防这种疾病具有重要意义。各种临床试验可用于测试抗氧化剂药物在青光眼管理中的功效。在这次审查中,我们讨论OS作为治疗靶点，提示促氧化剂/抗氧化剂状态的调节可能是青光眼预防和治疗的相关目标。
