Glaucoma and microglia-induced neuroinflammation
Glaucoma and microglia-induced neuroinflammation
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青光眼和小胶质细胞诱导的神经炎症
DOI：
10.3389/fopht.2023.1132011
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发表时间：
2023-02
期刊：
影响因子：
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通讯作者：
M. Ishikawa;Y. Izumi;Kota Sato;Taimu Sato;C. Zorumski;H. Kunikata;T. Nakazawa
中科院分区：
文献类型：
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作者：
M. Ishikawa;Y. Izumi;Kota Sato;Taimu Sato;C. Zorumski;H. Kunikata;T. Nakazawa
青光眼是一种多因素的神经退行性疾病，其特征是进行性视神经病变导致视野缺陷。眼压升高是青光眼发展的最大危险因素，而眼压降低是目前唯一可用的治疗方法。然而，在许多情况下，尽管眼压得到了足够的控制，视网膜退行性变仍会继续发展。因此，阐明青光眼抵抗当前降眼压治疗的病理生理学机制是很重要的。利用动物青光眼模型的实验表明，小胶质神经炎性反应与视网膜神经节细胞(RGCs)损伤之间的关系。抑制与小胶质细胞激活相关的神经炎性通路似乎具有神经保护作用，表明小胶质细胞可能是RGC保护的重要治疗靶点。在这篇综述中，我们将重点讨论小胶质细胞诱导的神经炎症在青光眼发病机制中的作用，以期为开发针对小胶质细胞的新型神经保护疗法的可能性提供新的见解。
Glaucoma is a multifactorial neurodegenerative disease characterized by a progressive optic neuropathy resulting in visual field defects. Elevated intraocular pressure (IOP) is the greatest risk factor for the development of glaucoma, and IOP reduction therapy is the only treatment currently available. However, there are many cases in which retinal degeneration progresses despite sufficient control of IOP. Therefore, it is important to elucidate the pathophysiology of glaucoma that is resistant to current IOP lowering therapies. Experiments using animal glaucoma models show the relationships between microglial neuroinflammatory responses and damage of retinal ganglion cells (RGCs). Inhibition of neuroinflammatory pathways associated with microglial activation appears to be neuroprotective, indicating that microglia may be an important therapeutic target for RGC protection. In this review, we will focus on microglia-induced neuroinflammation in the pathogenesis of glaucoma to offer new insights into the possibility of developing novel neuroprotective therapies targeting microglia.