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年龄相关性黄斑变性中的线粒体功能障碍与内质网应激:在病理生理学中的作用及可能的新治疗策略

Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Age Related Macular Degeneration, Role in Pathophysiology, and Possible New Therapeutic Strategies.

作者信息

Bilbao-Malavé Valentina, González-Zamora Jorge, de la Puente Miriam, Recalde Sergio, Fernandez-Robredo Patricia, Hernandez María, Layana Alfredo Garcia, Saenz de Viteri Manuel

机构信息

Department of Opthalmology, Clínica Universidad de Navarra, 31008 Pamplona, Spain.

Retinal Pathologies and New Therapies Group, Experimental Ophthalmology Laboratory, Department of Ophthalmology, Universidad de Navarra, 31008 Pamplona, Spain.

出版信息

Antioxidants (Basel). 2021 Jul 23;10(8):1170. doi: 10.3390/antiox10081170.

DOI:10.3390/antiox10081170
PMID:34439418
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8388889/
Abstract

Age related macular degeneration (AMD) is the main cause of legal blindness in developed countries. It is a multifactorial disease in which a combination of genetic and environmental factors contributes to increased risk of developing this vision-incapacitating condition. Oxidative stress plays a central role in the pathophysiology of AMD and recent publications have highlighted the importance of mitochondrial dysfunction and endoplasmic reticulum stress in this disease. Although treatment with vascular endothelium growth factor inhibitors have decreased the risk of blindness in patients with the exudative form of AMD, the search for new therapeutic options continues to prevent the loss of photoreceptors and retinal pigment epithelium cells, characteristic of late stage AMD. In this review, we explain how mitochondrial dysfunction and endoplasmic reticulum stress participate in AMD pathogenesis. We also discuss a role of several antioxidants (bile acids, resveratrol, melatonin, humanin, and coenzyme Q10) in amelioration of AMD pathology.

摘要

年龄相关性黄斑变性(AMD)是发达国家法定失明的主要原因。它是一种多因素疾病,遗传和环境因素共同作用会增加患这种导致视力丧失疾病的风险。氧化应激在AMD的病理生理学中起核心作用,最近的出版物强调了线粒体功能障碍和内质网应激在这种疾病中的重要性。尽管使用血管内皮生长因子抑制剂进行治疗已降低了渗出性AMD患者失明的风险,但寻找新的治疗选择仍在继续,以防止晚期AMD特有的光感受器和视网膜色素上皮细胞的丧失。在这篇综述中,我们解释了线粒体功能障碍和内质网应激如何参与AMD的发病机制。我们还讨论了几种抗氧化剂(胆汁酸、白藜芦醇、褪黑素、人胰岛素和辅酶Q10)在改善AMD病理方面的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/23e7775af32f/antioxidants-10-01170-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/7f2081712bd1/antioxidants-10-01170-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/d85689a0ff84/antioxidants-10-01170-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/1aaf47a054a1/antioxidants-10-01170-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/3e8c9a7f2dcf/antioxidants-10-01170-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/23e7775af32f/antioxidants-10-01170-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/7f2081712bd1/antioxidants-10-01170-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/d85689a0ff84/antioxidants-10-01170-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/1aaf47a054a1/antioxidants-10-01170-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/3e8c9a7f2dcf/antioxidants-10-01170-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3251/8388889/23e7775af32f/antioxidants-10-01170-g005.jpg

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