Oxidative stress in retinal pigment epithelium degeneration: from pathogenesis to therapeutic targets in dry age-related macular degeneration.
Oxidative stress in retinal pigment epithelium degeneration: from pathogenesis to therapeutic targets in dry age-related macular degeneration.
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视网膜色素上皮变性中的氧化应激：从发病机理到干燥年龄相关的黄斑变性的治疗靶标。
DOI：
10.4103/1673-5374.369098
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发表时间：
2023-10
影响因子：
6.1
通讯作者：
Chen J
中科院分区：
文献类型：
--
作者：
Maurya M;Bora K;Blomfield AK;Pavlovich MC;Huang S;Liu CH;Chen J
黄斑变性是老年人致盲的主要原因。过去几十年对该疾病的病理生理学的研究已经在针对新生血管性年龄相关性黄斑变性的抗血管内皮生长因子疗法的形式上取得了突破;然而，对于干性年龄相关性黄斑变性中的地理萎缩或防止年龄相关性黄斑变性从早期或中期进展到晚期，还没有有效的治疗方法。涉及人类年龄相关性黄斑变性视网膜和动物模型的临床和实验研究都指出视网膜色素上皮的萎缩性改变是年龄相关性黄斑变性进展的关键特征。视网膜色素上皮细胞主要负责细胞结构的维持和营养供应，以保持光感受器的健康和功能。视网膜色素上皮细胞持续承受高度氧化的环境，该环境与由核因子红细胞-2相关因子2作为主要氧化还原敏感转录因子调节的抗氧化酶系统级联平衡。衰老和累积的氧化应激触发视网膜色素上皮功能障碍并最终死亡。暴露于环境和遗传因素会加重老化视网膜色素上皮的氧化应激损伤，并加速年龄相关性黄斑变性病理生理学中的视网膜色素上皮变性。本文综述了氧化应激在视网膜色素上皮变性中的作用，以及遗传和环境因素对年龄相关性黄斑变性发生和进展的潜在影响。还讨论了通过增强其抗氧化能力来对抗视网膜色素上皮损伤和保护视网膜色素上皮的潜在策略，重点关注现有的抗氧化营养补充，并探索核因子红细胞2相关因子2及其调节因子包括REV-ERBα作为治疗靶点来预防年龄相关性黄斑变性的发展和进展。
Age-related macular degeneration is a primary cause of blindness in the older adult population. Past decades of research in the pathophysiology of the disease have resulted in breakthroughs in the form of anti-vascular endothelial growth factor therapies against neovascular age-related macular degeneration; however, effective treatment is not yet available for geographical atrophy in dry age-related macular degeneration or for preventing the progression from early or mid to the late stage of age-related macular degeneration. Both clinical and experimental investigations involving human age-related macular degeneration retinas and animal models point towards the atrophic alterations in retinal pigment epithelium as a key feature in age-related macular degeneration progression. Retinal pigment epithelium cells are primarily responsible for cellular-structural maintenance and nutrition supply to keep photoreceptors healthy and functional. The retinal pigment epithelium constantly endures a highly oxidative environment that is balanced with a cascade of antioxidant enzyme systems regulated by nuclear factor erythroid-2-related factor 2 as a main redox sensing transcription factor. Aging and accumulated oxidative stress triggers retinal pigment epithelium dysfunction and eventually death. Exposure to both environmental and genetic factors aggravates oxidative stress damage in aging retinal pigment epithelium and accelerates retinal pigment epithelium degeneration in age-related macular degeneration pathophysiology. The present review summarizes the role of oxidative stress in retinal pigment epithelium degeneration, with potential impacts from both genetic and environmental factors in age-related macular degeneration development and progression. Potential strategies to counter retinal pigment epithelium damage and protect the retinal pigment epithelium through enhancing its antioxidant capacity are also discussed, focusing on existing antioxidant nutritional supplementation, and exploring nuclear factor erythroid-2-related factor 2 and its regulators including REV-ERBα as therapeutic targets to protect against age-related macular degeneration development and progression.
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影响因子：
--
作者：
Cheng LB;Li KR;Yi N;Li XM;Wang F;Xue B;Pan YS;Yao J;Jiang Q;Wu ZF
通讯作者：
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Handa, James T.
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13.7
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