Bariş Mine, Tezel Gülgün
Columbia University, College of Physicians and Surgeons, Department of Ophthalmology, New York, NY.
Curr Ophthalmol Rep. 2019 Jun;7(2):160-169. Epub 2019 Apr 23.
This review aims to highlight the current knowledge about inflammatory mechanisms of neurodegeneration in glaucoma with emphasis on potential immunomodulation strategies.
Glaucomatous retina and optic nerve present multiple evidences of inflammatory responses of astroglia, microglia, and blood-born immune cells. Although adaptive/protective responses of resident or systemic immune cells can support neurons and promote tissue repair mechanisms after injurious insults, prolonged inflammatory processes can also produce neurotoxic mediators. Treatments targeting these neurodestructive outcomes may restore immune homeostasis and protect neurons from inflammatory injury. Due to widespread and chronic nature of neuroinflammation in glaucoma, immunomodulation offers a treatment strategy to protect different neuronal compartments of RGCs during the chronic and asynchronous course of neurodegeneration. Uncovering of distinct molecular responses and interactions of different immune cells that determine the neuroinflammatory phenotype and participate in neurodegenerative outcomes will be critical to develop effective strategies for immunomodulation in glaucoma.
Neuroinflammation has increasingly been recognized to play an important role in glaucomatous neurodegeneration, and its modulation appears to be a promising treatment strategy for neuroprotection.
本综述旨在强调目前关于青光眼神经退行性变炎症机制的认识,重点关注潜在的免疫调节策略。
青光眼患者的视网膜和视神经呈现出星形胶质细胞、小胶质细胞和血源性免疫细胞炎症反应的多种证据。尽管驻留或全身免疫细胞的适应性/保护性反应可在损伤性刺激后支持神经元并促进组织修复机制,但长期的炎症过程也可产生神经毒性介质。针对这些神经破坏性后果的治疗可能恢复免疫稳态并保护神经元免受炎症损伤。由于青光眼神经炎症具有广泛和慢性的特点,免疫调节提供了一种治疗策略,可在神经退行性变的慢性和异步过程中保护视网膜神经节细胞的不同神经元成分。揭示决定神经炎症表型并参与神经退行性变结果的不同免疫细胞的独特分子反应和相互作用,对于制定有效的青光眼免疫调节策略至关重要。
神经炎症在青光眼性神经退行性变中日益被认为起着重要作用,对其进行调节似乎是一种有前景的神经保护治疗策略。