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光暴露视网膜中的氧化应激及其在年龄相关性黄斑变性中的意义。

Oxidative stress in the light-exposed retina and its implication in age-related macular degeneration.

机构信息

St Luke's International University, Department of Ophthalmology, St Luke's International Hospital, 9-1 Akashi-cho, Chuo-ku, Tokyo, 104-8560, Japan; Laboratory of Retinal Cell Biology, Department of Ophthalmology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.

出版信息

Redox Biol. 2020 Oct;37:101779. doi: 10.1016/j.redox.2020.101779. Epub 2020 Nov 2.

DOI:10.1016/j.redox.2020.101779
PMID:33172789
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7767731/
Abstract

The retina continuously receives light to enable vision, and the related processes require a marked amount of energy. During active metabolism, reactive oxygen species (ROS) are generated in exchange. Although physiologically generated ROS may be removed by endogenous antioxidant systems, and the effects of oxidative stress may be recovered by repair systems to retain homeostasis and health, when ROS and oxidative stress exceed the capacity of the antioxidant and repair systems, the condition becomes pathological. Multiple mechanisms of oxidative stress and the effects of antioxidant and repair systems in the retina have long been analyzed using light-induced retinal degeneration models. Among the mechanisms, a positive feedback loop of oxidative stress and related inflammation may be involved in the pathogenesis of a blinding aging disease, age-related macular degeneration. Treatments for suppressing ROS and oxidative stress by administrating antioxidant products may support the tissue-protective function of antioxidant systems. Moreover, recent studies have proposed a new concept for maintaining homeostasis by supplying sufficient energy to activate the repair systems. The current review will help elucidate the influence of oxidative stress and guide future analyses to explore new therapeutic approaches for oxidative stress-mediated diseases.

摘要

视网膜不断接收光线以实现视觉,相关过程需要大量的能量。在此过程中,会产生活性氧(ROS)作为交换。虽然生理产生的 ROS 可以被内源性抗氧化系统清除,氧化应激的影响也可以通过修复系统恢复来维持体内平衡和健康,但当 ROS 和氧化应激超过抗氧化和修复系统的能力时,就会出现病理状态。长期以来,人们一直在使用光诱导的视网膜变性模型来分析氧化应激的多种机制以及视网膜中抗氧化和修复系统的作用。在这些机制中,氧化应激和相关炎症的正反馈循环可能参与了致盲性衰老疾病——年龄相关性黄斑变性的发病机制。通过给予抗氧化产品来抑制 ROS 和氧化应激的治疗方法可能支持抗氧化系统的组织保护功能。此外,最近的研究提出了通过提供足够的能量激活修复系统来维持体内平衡的新概念。本综述将有助于阐明氧化应激的影响,并为探索氧化应激介导疾病的新治疗方法提供指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/d52bb88a110b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/dcf4061d022c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/c8b8695a284c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/c2544f21096e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/234c6f562a16/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/d52bb88a110b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/dcf4061d022c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/c8b8695a284c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/c2544f21096e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/234c6f562a16/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1191/7767731/d52bb88a110b/gr5.jpg

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