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肠道-视网膜轴:揭示自身免疫在青光眼发病中的作用。

The gut-retina axis: Uncovering the role of autoimmunity in glaucoma development.

作者信息

Yang Zuyi, Tian Dianzhe, Zhao Xinyu, Luo Yunping, Chen Youxin

机构信息

Eight-year Medical Doctor Program, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, 100730, China.

出版信息

Heliyon. 2024 Aug 3;10(15):e35516. doi: 10.1016/j.heliyon.2024.e35516. eCollection 2024 Aug 15.

Abstract

Glaucoma, a leading cause of irreversible blindness worldwide, is characterized by progressive loss of retinal ganglion cells (RGCs) and optic nerve damage. While elevated intraocular pressure (IOP) is the only known modifiable risk factor, normal-tension glaucoma (NTG) challenges this notion, suggesting other mechanisms beyond IOP may contribute to its development. Emerging evidence support the hypothesis that glaucoma may be an autoimmune disease. This review summarizes evidence for this hypothesis, focusing on the gut-retina axis. We discuss how antigens of gut bacterial prime peripheral T cells to breach the blood-retina barrier (BRB) and initiate cross-reactivity with ocular tissues via molecular mimicry, resulting in autoimmune RGC damage. Understanding these mechanisms may uncover new diagnostic biomarkers and therapeutic strategies targeting immune pathways alongside conventional IOP-lowering treatments.

摘要

青光眼是全球不可逆性失明的主要原因,其特征是视网膜神经节细胞(RGCs)逐渐丧失和视神经损伤。虽然眼压升高(IOP)是唯一已知的可改变风险因素,但正常眼压性青光眼(NTG)对这一观点提出了挑战,表明眼压以外的其他机制可能有助于其发展。新出现的证据支持青光眼可能是一种自身免疫性疾病的假说。本综述总结了这一假说的证据,重点关注肠-视网膜轴。我们讨论了肠道细菌抗原如何激活外周T细胞,使其突破血视网膜屏障(BRB),并通过分子模拟与眼组织引发交叉反应,从而导致自身免疫性RGC损伤。了解这些机制可能会发现新的诊断生物标志物和治疗策略,除了传统的降低眼压治疗外,还可针对免疫途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe19/11336731/a74dffd0f310/ga1.jpg

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