Schepens Eye Research Institute of Mass Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
Animal Physiology/Neurobiology, Department of Biology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91058 Erlangen, Germany.
Int J Mol Sci. 2024 Feb 15;25(4):2307. doi: 10.3390/ijms25042307.
Glaucoma is a progressive neurodegenerative disease characterized by damage to the optic nerve that results in irreversible vision loss. While the exact pathology of glaucoma is not well understood, emerging evidence suggests that dysregulation of the complement system, a key component of innate immunity, plays a crucial role. In glaucoma, dysregulation of the complement cascade and impaired regulation of complement factors contribute to chronic inflammation and neurodegeneration. Complement components such as C1Q, C3, and the membrane attack complex have been implicated in glaucomatous neuroinflammation and retinal ganglion cell death. This review will provide a summary of human and experimental studies that document the dysregulation of the complement system observed in glaucoma patients and animal models of glaucoma driving chronic inflammation and neurodegeneration. Understanding how complement-mediated damage contributes to glaucoma will provide opportunities for new therapies.
青光眼是一种进行性神经退行性疾病，其特征是视神经损伤，导致不可逆转的视力丧失。尽管青光眼的确切病理机制尚不清楚，但新出现的证据表明，补体系统的失调，即先天免疫的一个关键组成部分，起着至关重要的作用。在青光眼，补体级联失调和补体因子调节受损导致慢性炎症和神经退行性变。补体成分如 C1Q、C3 和膜攻击复合物已被牵连到青光眼神经炎症和视网膜神经节细胞死亡中。本综述将总结人类和实验研究，记录在青光眼患者和青光眼动物模型中观察到的补体系统失调，驱动慢性炎症和神经退行性变。了解补体介导的损伤如何导致青光眼，将为新疗法提供机会。
