Wang Minwei, Su Shiqi, Jiang Shaoyun, Sun Xinghuai, Wang Jiantao
Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California, USA.
Department of Anatomy and Neurobiology, University of California Irvine, Irvine, California, USA.
BMJ Open Ophthalmol. 2021 Jun 29;6(1):e000774. doi: 10.1136/bmjophth-2021-000774. eCollection 2021.
Age-related macular degeneration (AMD) is the most common eye disease in elderly patients, which could lead to irreversible vision loss and blindness. Increasing evidence indicates that amyloid β-peptide (Aβ) might be associated with the pathogenesis of AMD. In this review, we would like to summarise the current findings in this field. The literature search was done from 1995 to Feb, 2021 with following keywords, 'Amyloid β-peptide and age-related macular degeneration', 'Inflammation and age-related macular degeneration', 'Angiogenesis and age-related macular degeneration', 'Actin cytoskeleton and amyloid β-peptide', 'Mitochondrial dysfunction and amyloid β-peptide', 'Ribosomal dysregulation and amyloid β-peptide' using search engines Pubmed, Google Scholar and Web of Science. Aβ congregates in subretinal drusen of patients with AMD and participates in the pathogenesis of AMD through enhancing inflammatory activity, inducing mitochondrial dysfunction, altering ribosomal function, regulating the lysosomal pathway, affecting RNA splicing, modulating angiogenesis and modifying cell structure in AMD. The methods targeting Aβ are shown to inhibit inflammatory signalling pathway and restore the function of retinal pigment epithelium cells and photoreceptor cells in the subretinal region. Targeting Aβ may provide a novel therapeutic strategy for AMD.
年龄相关性黄斑变性(AMD)是老年患者中最常见的眼病,可导致不可逆的视力丧失和失明。越来越多的证据表明,淀粉样β肽(Aβ)可能与AMD的发病机制有关。在本综述中,我们将总结该领域的当前研究结果。使用搜索引擎PubMed、谷歌学术和科学网,以“淀粉样β肽与年龄相关性黄斑变性”、“炎症与年龄相关性黄斑变性”、“血管生成与年龄相关性黄斑变性”、“肌动蛋白细胞骨架与淀粉样β肽”、“线粒体功能障碍与淀粉样β肽”、“核糖体失调与淀粉样β肽”为关键词,进行了从1995年至2021年2月的文献检索。Aβ在AMD患者的视网膜下玻璃膜疣中聚集,并通过增强炎症活性、诱导线粒体功能障碍、改变核糖体功能、调节溶酶体途径、影响RNA剪接、调节血管生成和改变AMD中的细胞结构来参与AMD的发病机制。针对Aβ的方法显示可抑制炎症信号通路,并恢复视网膜色素上皮细胞和视网膜下区域光感受器细胞的功能。针对Aβ可能为AMD提供一种新的治疗策略。