Activated Retinal Pigment Epithelium, an Optical Coherence Tomography Biomarker for Progression in Age-Related Macular Degeneration.
Activated Retinal Pigment Epithelium, an Optical Coherence Tomography Biomarker for Progression in Age-Related Macular Degeneration.
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DOI：
10.1167/iovs.17-21872
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发表时间：
2017-05-01
影响因子：
4.4
通讯作者：
Freund KB
中科院分区：
文献类型：
--
作者：
Curcio CA;Zanzottera EC;Ach T;Balaratnasingam C;Freund KB
总结和介绍近年来关于视网膜色素上皮(RPE)在晚期老年性黄斑变性(AMD)中的命运的组织学和临床影像文献；支持RPE的激活和迁移是萎缩的重要先兆，在光谱域光学相干断层扫描(SDOCT)中表现为视网膜内的高反射灶。对AMD组织病理学的Project macula在线资源进行了系统的调查，形成了晚期疾病中RPE和RPE来源的细胞的15种表型和层厚度的目录。表型与临床纵向眼球追踪的SDOCT以及与地理萎缩(GA)和色素上皮脱离(PED)的体外影像-组织病理学的相关性也被寻找。形态分类表明RPE命运的两条主要途径：细胞内细胞器的基底外侧脱落(明显的原位凋亡)和激活的前向迁移。获得性卵黄样病变可能是第三种途径。迁移的细胞被RPE细胞器包裹，并在SDOCT上确认为高反射。在GA边界附近，由于细胞变形和厚层基底层沉积，RPE层增厚。视网膜色素变性表现为一个缓慢生长和快速崩溃的生命周期，在此之前，RPE层破裂和前向迁移。RPE的激活和迁移是萎缩的重要前兆，通过验证的SDOCT可以在体内的细胞水平观察到这种现象。当RPE死亡和迁移阻止Druse组分的继续生产时，似乎会发生大的玻璃体和葡萄膜样PED的崩溃。数据表明在RPE死亡中与脉络膜毛细血管的扩散距离过远，并支持在GA中靶向玻璃体的潜在益处。
To summarize and contextualize recent histology and clinical imaging publications on retinal pigment epithelium (RPE) fate in advanced age-related macular degeneration (AMD); to support RPE activation and migration as important precursors to atrophy, manifest as intraretinal hyperreflective foci in spectral-domain optical coherence tomography (SDOCT). The Project MACULA online resource for AMD histopathology was surveyed systematically to form a catalog of 15 phenotypes of RPE and RPE-derived cells and layer thicknesses in advanced disease. Phenotypes were also sought in correlations with clinical longitudinal eye-tracked SDOCT and with ex vivo imaging–histopathology correlations in geographic atrophy (GA) and pigment epithelium detachments (PED). The morphology catalog suggested two main pathways of RPE fate: basolateral shedding of intracellular organelles (apparent apoptosis in situ) and activation with anterior migration. Acquired vitelliform lesions may represent a third pathway. Migrated cells are packed with RPE organelles and confirmed as hyperreflective on SDOCT. RPE layer thickening due to cellular dysmorphia and thick basal laminar deposit is observed near the border of GA. Drusenoid PED show a life cycle of slow growth and rapid collapse preceded by RPE layer disruption and anterior migration. RPE activation and migration comprise an important precursor to atrophy that can be observed at the cellular level in vivo via validated SDOCT. Collapse of large drusen and drusenoid PED appears to occur when RPE death and migration prevent continued production of druse components. Data implicate excessive diffusion distance from choriocapillaris in RPE death as well as support a potential benefit in targeting drusen in GA.