Zhao Xiaohuan, Sun Rou, Luo Xueting, Wang Feng, Sun Xiaodong
Shanghai Key Laboratory of Ocular Fundus Diseases, Shanghai General Hospital, Shanghai Engineering Center for Visual Science and Photomedicine, Shanghai, China.
Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Front Neurosci. 2021 May 28;15:610788. doi: 10.3389/fnins.2021.610788. eCollection 2021.
Glaucoma, a neurodegenerative disease that leads to irreversible vision loss, is characterized by progressive loss of retinal ganglion cells (RGCs) and optic axons. To date, elevated intraocular pressure (IOP) has been recognized as the main phenotypic factor associated with glaucoma. However, some patients with normal IOP also have glaucomatous visual impairment and RGC loss. Unfortunately, the underlying mechanisms behind such cases remain unclear. Recent studies have suggested that retinal glia play significant roles in the initiation and progression of glaucoma. Multiple types of glial cells are activated in glaucoma. Microglia, for example, act as critical mediators that orchestrate the progression of neuroinflammation through pro-inflammatory cytokines. In contrast, macroglia (astrocytes and Müller cells) participate in retinal inflammatory responses as modulators and contribute to neuroprotection through the secretion of neurotrophic factors. Notably, research results have indicated that intricate interactions between microglia and macroglia might provide potential therapeutic targets for the prevention and treatment of glaucoma. In this review, we examine the specific roles of microglia and macroglia in open-angle glaucoma, including glaucoma in animal models, and analyze the interaction between these two cell types. In addition, we discuss potential treatment options based on the relationship between glial cells and neurons.
青光眼是一种导致不可逆视力丧失的神经退行性疾病,其特征是视网膜神经节细胞(RGCs)和视神经轴突逐渐丧失。迄今为止,眼压升高已被公认为与青光眼相关的主要表型因素。然而,一些眼压正常的患者也存在青光眼性视力损害和RGC丧失。不幸的是,此类病例背后的潜在机制仍不清楚。最近的研究表明,视网膜神经胶质细胞在青光眼的发生和发展中起重要作用。青光眼会激活多种类型的神经胶质细胞。例如,小胶质细胞作为关键介质,通过促炎细胞因子协调神经炎症的进展。相比之下,大胶质细胞(星形胶质细胞和穆勒细胞)作为调节因子参与视网膜炎症反应,并通过分泌神经营养因子促进神经保护。值得注意的是,研究结果表明,小胶质细胞和大胶质细胞之间复杂的相互作用可能为青光眼的预防和治疗提供潜在的治疗靶点。在这篇综述中,我们研究了小胶质细胞和大胶质细胞在开角型青光眼中的具体作用,包括动物模型中的青光眼,并分析了这两种细胞类型之间的相互作用。此外,我们还根据神经胶质细胞与神经元之间的关系讨论了潜在的治疗选择。