青光眼中神经退行性病变的机制研究和治疗进展  

Pathogenesis and therapeutic advances of neurodegenerationin glaucoma

作　　者：曹迎雪 麦小妹(综述) 石乐 徐明明 孙泽惠 柳夏林[1] 易薇(审校) CAO Yingxue;MAI Xiaomei;SHI Le;XU Mingming;SUN Zehui;LIU Xialin;YI Wei(State Key Laboratory of Ophthalmology,Zhongshan Ophthalmic Center,Sun Yat-sen University,Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science,Guangzhou 510060,China)

机构地区：[1]中山大学中山眼科中心,眼病防治全国重点实验室,广东省眼科视觉科学重点实验室,广州510060

出　　处：《眼科学报》2024年第8期402-408,共7页Eye Science

基　　金：国家自然科学基金(82101329,82271095);广东省重点领域研发计划(2023B1111050004);广州市科技计划项目(2024B01J1121)。

摘　　要：青光眼是全球第一大不可逆性致盲性眼病,影响全球7000多万人,其特征是视网膜神经节细胞的退行性病变。到2040年,预计全球青光眼患者人数将增加至1.12亿,其中约10%的人至少一只眼睛失明。由高眼压诱发、多种致病因素导致的视网膜神经节细胞死亡是青光眼进展过程中视功能损伤的主要病理过程,也是青光眼病程中视功能损害不可逆的重要原因。目前降眼压治疗是唯一的干预疗法,然而其仍然不能完全遏止视网膜神经节细胞进行性损伤,并且既往病程造成的视神经损伤不可逆转。探索青光眼进程中视网膜神经节细胞退行性改变的直接致病因素,寻找关键的治疗靶点,以及开发新的具有神经保护作用的治疗药物,具有重要意义。文章回顾了近年来青光眼中视网膜神经节细胞退行性病变的机制和治疗的新进展,强调了神经血管单元的改变在青光眼发病机制中的重要作用和干预价值。同时,靶向代谢的药物应用、抑制早期炎症反应和减少氧化应激,辅以营养和运动支持等可能延缓和抑制神经退行性病变的发生,起到神经保护作用。未来青光眼发病机制的研究重点仍然在眼压之外的致病因素上,从血流、代谢和免疫串扰的病理环境中发掘对神经退行性改变重要的致病因素并进行干预治疗具有广阔的前景。在多种动物模型中验证干预手段的神经保护作用,也有望提高青光眼神经保护的临床转化成功率,以拓展青光眼的治疗理念与药物选择。Glaucoma stands as the leading cause of irreversible blindness globally,affecting over 70 million individuals.It is characterized by progressive degeneration of retinal ganglion cells(RGCs).By 2040,the global prevalence of glaucoma is expected to rise to 112 million,with approximately 10%experiencing blindness in at least one eye.The primary pathological basis for visual function impairment in glaucoma progression is the loss of RGCs induced by elevated intraocular pressure(IOP)and various pathogenic factors.Currently,IOP-lowering treatment is the only intervention available,but it cannot completely halt the progressive injury to RGCs,nor can it reverse the optic nerve damage caused by prior disease progression.Exploring the direct pathogenic factors of RGC degeneration in glaucoma,identifying key therapeutic targets,and developing new neuroprotective treatments are of great importance.This review discusses recent advancements in the mechanisms and treatments of retinal ganglion cell degeneration in glaucoma,highlighting the significant role of neurovascular unit changes in the pathogenesis of glaucoma and the potential value of interventions.Additionally,targeting metabolites,inhibiting early inflammatory responses,and reducing oxidative stress,supplemented by nutritional and exercise support,may help delay and inhibit neurodegenerative processes,offering neuroprotective effects.Future research on glaucoma pathogenesis should focus on factors beyond IOP,exploring pathogenic factors in the pathological environment of blood flow,metabolism,and immune crosstalk for targeted therapeutic interventions.Also,verifying the neuroprotective effects of these interventions in various animal models holds promise for improving the clinical translation success rate of neuroprotection in glaucoma,thus expanding therapeutic concepts and drug options.

关 键 词：青光眼 视网膜神经节细胞 高眼压 神经保护 治疗进展 

分 类 号：R775[医药卫生—眼科]