NF-κB 对老年性黄斑变性的炎症和血管生成过程的影响

IF 3 2区 医学 Q1 OPHTHALMOLOGY
Waleed Hassan Almalki , Salem Salman Almujri
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引用次数: 0

摘要

老年性黄斑变性(AMD)是导致视力下降的主要原因,分为干性(萎缩性)和湿性(新生血管性)两种不同类型。干性黄斑变性的特点是视网膜细胞逐渐退化,最终导致视力下降。相比之下,湿性老年黄斑变性是指视网膜下的血管发育异常,导致视力突然严重受损。老年性黄斑变性的病程主要由慢性炎症和病理性血管生成驱动,其中 NF-κB 信号通路起着至关重要的作用。NF-κB 的激活导致促炎细胞因子、趋化因子和血管生成因子(如血管内皮生长因子)的产生,这些因子有助于炎症和新血管在 AMD 中的形成。本综述分析了 AMD 中 NF-κB 信号传导、炎症和血管生成之间错综复杂的关系,并评估了将 NF-κB 作为治疗靶点的可能性。该评估包括对临床前和临床证据的全面检查,这些证据证实了NF-κB抑制剂通过减少炎症和病理性血管生成来治疗AMD的有效性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The impact of NF-κB on inflammatory and angiogenic processes in age-related macular degeneration
Age-related macular degeneration (AMD) is a prominent cause of vision loss, characterized by two different types, dry (atrophic) and wet (neovascular). Dry AMD is distinguished by the progressive deterioration of retinal cells, which ultimately causes a decline in vision. In contrast, wet AMD is defined by the abnormal development of blood vessels underneath the retina, leading to a sudden and severe vision impairment. The course of AMD is primarily driven by chronic inflammation and pathological angiogenesis, in which the NF-κB signaling pathway plays a crucial role. The activation of NF-κB results in the generation of pro-inflammatory cytokines, chemokines, and angiogenic factors like VEGF, which contribute to inflammation and the formation of new blood vessels in AMD. This review analyzes the intricate relationship between NF-κB signaling, inflammation, and angiogenesis in AMD and assesses the possibility of using NF-κB as a target for therapy. The evaluation involves a comprehensive examination of preclinical and clinical evidence that substantiates the effectiveness of NF-κB inhibitors in treating AMD by diminishing inflammation and pathological angiogenesis.
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来源期刊
Experimental eye research
Experimental eye research 医学-眼科学
CiteScore
6.80
自引率
5.90%
发文量
323
审稿时长
66 days
期刊介绍: The primary goal of Experimental Eye Research is to publish original research papers on all aspects of experimental biology of the eye and ocular tissues that seek to define the mechanisms of normal function and/or disease. Studies of ocular tissues that encompass the disciplines of cell biology, developmental biology, genetics, molecular biology, physiology, biochemistry, biophysics, immunology or microbiology are most welcomed. Manuscripts that are purely clinical or in a surgical area of ophthalmology are not appropriate for submission to Experimental Eye Research and if received will be returned without review.
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