Kimura Atsuko, Namekata Kazuhiko, Guo Xiaoli, Noro Takahiko, Harada Chikako, Harada Takayuki
Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Oxid Med Cell Longev. 2017;2017:2817252. doi: 10.1155/2017/2817252. Epub 2017 Feb 8.
Glaucoma is a neurodegenerative disease of the eye and it is one of the leading causes of blindness. Glaucoma is characterized by progressive degeneration of retinal ganglion cells (RGCs) and their axons, namely, the optic nerve, usually associated with elevated intraocular pressure (IOP). Current glaucoma therapies target reduction of IOP, but since RGC death is the cause of irreversible vision loss, neuroprotection may be an effective strategy for glaucoma treatment. One of the risk factors for glaucoma is increased oxidative stress, and drugs with antioxidative properties including valproic acid and spermidine, as well as inhibition of apoptosis signal-regulating kinase 1, an enzyme that is involved in oxidative stress, have been reported to prevent glaucomatous retinal degeneration in mouse models of glaucoma. Optic neuritis is a demyelinating inflammation of the optic nerve that presents with visual impairment and it is commonly associated with multiple sclerosis, a chronic demyelinating disease of the central nervous system. Although steroids are commonly used for treatment of optic neuritis, reduction of oxidative stress by approaches such as gene therapy is effective in ameliorating optic nerve demyelination in preclinical studies. In this review, we discuss oxidative stress as a therapeutic target for glaucoma and optic neuritis.
青光眼是一种眼部神经退行性疾病，是导致失明的主要原因之一。青光眼的特征是视网膜神经节细胞（RGCs）及其轴突（即视神经）进行性退化，通常与眼内压（IOP）升高有关。目前的青光眼治疗方法旨在降低眼内压，但由于RGC死亡是不可逆视力丧失的原因，神经保护可能是治疗青光眼的有效策略。青光眼的危险因素之一是氧化应激增加，据报道，具有抗氧化特性的药物（包括丙戊酸和亚精胺）以及抑制参与氧化应激的凋亡信号调节激酶1，可在青光眼小鼠模型中预防青光眼性视网膜变性。视神经炎是一种视神经脱髓鞘炎症，表现为视力障碍，通常与多发性硬化症有关，多发性硬化症是一种中枢神经系统慢性脱髓鞘疾病。尽管类固醇常用于治疗视神经炎，但在临床前研究中，通过基因治疗等方法降低氧化应激可有效改善视神经脱髓鞘。在这篇综述中，我们讨论了氧化应激作为青光眼和视神经炎的治疗靶点。
