基因疗法如何改变我们治疗老年性黄斑变性的方式?

Pub Date : 2022-11-02 DOI:10.1080/17469899.2022.2147927

Huma Khan, Hannah Khan, A. Aziz, Tyler M Ewing, A. Khanani

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引用次数: 1

摘要

年龄相关性黄斑变性（AMD）是50岁以上个体永久性视力丧失的主要原因[1]。晚期AMD在解剖学上可以表现为新生血管性AMD或萎缩性AMD。nAMD表现出源自脉络膜或视网膜的异常血管系统的特征性生长，导致黄斑新生血管形成（MNV）。MNV进展可导致光感受器退化、黄斑损伤和视网膜色素上皮破裂[1]。如果不及时治疗，nAMD中的MNV会导致液体、脂质和血液泄漏到视网膜外层，导致不可逆的视力丧失[1]。萎缩性AMD可发展为地理性萎缩（GA），其特征是绒毛膜毛细血管、视网膜色素上皮细胞和黄斑光感受器萎缩[1]。

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How could gene therapy change the way we treat age-related macular degeneration?

Age-related macular degeneration (AMD) is the leading cause of permanent vision loss in individuals over 50 years of age [1]. Advanced AMD can anatomically present as either neovascular (nAMD) or atrophic AMD. nAMD displays characteristic growth of abnormal vasculature that originates from the choroid or retina, resulting in macular neovascularization (MNV). MNV progression can lead to degeneration of photoreceptors, macular damage, and retinal pigment epithelium disruption [1]. If left untreated, MNV in nAMD can lead to leakage of fluid, lipid, and blood into the outer retina, resulting in irreversible vision loss [1]. Atrophic AMD can progress to geographic atrophy (GA), characterized by atrophy of choriocapillaris, retinal pigment epithelial cells, and macular photoreceptors [1].

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