炎症在近视视网膜病变中的作用。

IF 0.9
Frontiers in ophthalmology Pub Date : 2025-08-20 eCollection Date: 2025-01-01 DOI:10.3389/fopht.2025.1632047
Tianxiang Yang, Jinyan Qi, Heping Xu
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引用次数: 0

摘要

高度近视是一个全球性的健康问题,经常导致视网膜退行性改变,即近视性视网膜病变。虽然机械应力、低灌注、细胞外基质重塑和生长因子失调与近视视网膜病变的发病机制有关,但新出现的证据强调了慢性低度炎症的关键作用。先天免疫系统和适应性免疫系统通过全身和局部炎症参与近视视网膜病变。在系统上,免疫失调的标志是补体蛋白C3水平升高,抗lim和衰老nt细胞抗原样结构域蛋白1(抗lims1)的自身抗体水平升高,循环免疫细胞改变(中性粒细胞和嗜碱性粒细胞增加)。局部,视网膜稳态破坏触发眼内炎症,表现为白细胞介素-6 (IL-6)、IL-8、肿瘤坏死因子α (TNF-α)、C-C基序趋化因子配体2 (CCL2)、C-X-C基序趋化因子配体10 (CXCL10)水平升高,并激活补体系统。炎症反应涉及信号通路,如JAK-STAT和补体级联。本文综述了近视眼视网膜病变免疫机制的研究进展,为今后的研究提供指导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The role of inflammation in myopic retinopathy.

The role of inflammation in myopic retinopathy.

High myopia is a global health concern, often leading to degenerative retinal changes known as myopic retinopathy. Although mechanical stress, hypoperfusion, extracellular matrix remodeling, and growth factor dysregulation have been implicated in the pathogenesis of myopic retinopathy, emerging evidence highlights the critical role of chronic low-grade inflammation. Both innate and adaptive immune systems participate in myopic retinopathy through systemic and local inflammation. Systemically, immune dysregulation is marked by elevated levels of complement proteins C3, autoantibodies anti-LIM and senesce nt cell antigen-like-containing domain protein 1 (anti-LIMS1), and altered circulating immune cells (increased neutrophils and basophils). Locally, retinal homeostasis disruption triggers intraocular inflammation, evidenced by higher levels of interleukin-6 (IL-6), IL-8, tumor necrosis factor α (TNF-α), C-C motif chemokine ligand-2 (CCL2), C-X-C motif chemokine ligand 10 (CXCL10) and activating the complement system. The inflammatory response involves signaling pathways such as JAK-STAT and complement cascades. This review summarizes recent advances in understanding immunological mechanisms underlying myopic retinopathy, offering insights to guide future research.

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