褪黑素
氧化应激
黄斑变性
线粒体
线粒体生物发生
视网膜色素上皮
生物
线粒体DNA
活性氧
细胞生物学
视网膜变性
线粒体ROS
炎症
视网膜
内科学
内分泌学
医学
免疫学
神经科学
遗传学
眼科
基因
作者
Saeed Mehrzadi,Karim Hemati,Rüssel J. Reiter,Azam Hosseinzadeh
标识
DOI:10.1080/14728222.2020.1737015
摘要
Introduction: Age-related Macular Degeneration (AMD), a retinal neurodegenerative disease is the most common cause of blindness among the elderly in developed countries. The impairment of mitochondrial biogenesis has been reported in human retinal pigment epithelium (RPE) cells affected by AMD. Oxidative/nitrosative stress plays an important role in AMD development. The mitochondrial respiratory system is considered a major site of reactive oxygen species (ROS) generation. During aging, insufficient free radical scavenger systems, impairment of DNA repair mechanisms and reduction of mitochondrial degradation and turnover contribute to the massive accumulation of ROS disrupting mitochondrial function. Impaired mitochondrial function leads to the decline in the autophagic capacity and induction of inflammation and apoptosis in human RPE cells affected by AMD.Areas covered: This article evaluates the ameliorative effect of melatonin on AMD and examines AMD pathogenesis with an emphasis on mitochondrial dysfunction. It also considers the potential effects of melatonin on mitochondrial function.Expert opinion: The effect of melatonin on mitochondrial function results in the reduction of oxidative stress, inflammation and apoptosis in the retina; these findings demonstrate that melatonin has the potential to prevent and treat AMD.
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