视网膜色素上皮细胞因氧化应激及年龄相关性黄斑变性而发生坏死性凋亡。
RPE necroptosis in response to oxidative stress and in AMD.
作者信息
Hanus Jakub, Anderson Chastain, Wang Shusheng
机构信息
Department of Cell and Molecular Biology, Tulane University, New Orleans, LA 70118, USA.
Department of Cell and Molecular Biology, Tulane University, New Orleans, LA 70118, USA; Department of Ophthalmology, Tulane University, New Orleans, LA 70118, USA.
出版信息
Ageing Res Rev. 2015 Nov;24(Pt B):286-98. doi: 10.1016/j.arr.2015.09.002. Epub 2015 Sep 11.
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly. The underlying mechanism of non-neovascular AMD (dry AMD), also named geographic atrophy (GA) remains unclear and the mechanism of retinal pigment epithelial (RPE) cell death in AMD is controversial. We review the history and recent progress in understanding the mechanism of RPE cell death induced by oxidative stress, in AMD mouse models, and in AMD patients. Due to the limitation of toolsets to distinguish between apoptosis and necroptosis (or necrosis), most previous research concludes that apoptosis is a major mechanism for RPE cell death in response to oxidative stress and in AMD. Recent studies suggest necroptosis as a major mechanism of RPE cell death in response to oxidative stress. Moreover, ultrastructural and histopathological studies support necrosis as major mechanism of RPE cells death in AMD. In this review, we discuss the mechanism of RPE cell death in response to oxidative stress, in AMD mouse models, and in human AMD patients. Based on the literature, we hypothesize that necroptosis is a major mechanism for RPE cell death in response to oxidative stress and in AMD.
年龄相关性黄斑变性（AMD）是老年人不可逆失明的主要原因。非新生血管性AMD（干性AMD），也称为地图样萎缩（GA）的潜在机制仍不清楚，且AMD中视网膜色素上皮（RPE）细胞死亡的机制存在争议。我们回顾了在理解氧化应激诱导的RPE细胞死亡机制、AMD小鼠模型以及AMD患者方面的历史和最新进展。由于区分凋亡和坏死性凋亡（或坏死）的工具集有限，大多数先前的研究得出结论，凋亡是RPE细胞在氧化应激和AMD中死亡的主要机制。最近的研究表明坏死性凋亡是RPE细胞在氧化应激下死亡的主要机制。此外，超微结构和组织病理学研究支持坏死是AMD中RPE细胞死亡的主要机制。在本综述中，我们讨论了氧化应激、AMD小鼠模型以及人类AMD患者中RPE细胞死亡的机制。基于文献，我们假设坏死性凋亡是RPE细胞在氧化应激和AMD中死亡的主要机制。
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