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施万细胞通过减轻氧化应激介导视网膜退行性疾病中的视力保护:一种可能的机制。

Schwann Cell-Mediated Preservation of Vision in Retinal Degenerative Diseases via the Reduction of Oxidative Stress: A Possible Mechanism.

作者信息

Mahmoudzadeh Raziyeh, Heidari-Keshel Saeed, Lashay Alireza

机构信息

Stem Cell Preparation Unit, Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Iran.

出版信息

Med Hypothesis Discov Innov Ophthalmol. 2016 Summer;5(2):47-52.

PMID:28293647
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5347187/
Abstract

After injury to the central nervous system (CNS), regeneration is often inadequate, except in the case of remyelination. This remyelination capacity of the CNS is a good example of a stem/precursor cell-mediated renewal process. Schwann cells have been found to act as remyelinating agents in the peripheral nervous system (PNS), but several studies have highlighted their potential role in remyelination in the CNS too. Schwann cells are able to protect and support retinal cells by secreting growth factors such as brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, and basic fibroblast growth factor. Retinal degenerative diseases can be highly debilitating, and they are a major concern in countries with an ageing populations. One of the leading causes of permanent loss of vision in the West is a retinal degenerative disease known as age-related macular degeneration (AMD). In the United States, nearly 1.75 million people over the age of 40 have advanced AMD, and it is estimated that this number will increase to approximately 3 million people by 2020. One of the most common pathways involved in the initiation and development of retinal diseases is the oxidative stress pathway. In patients with diabetes, Schwann cells have been shown to be able to secrete large amounts of antioxidant enzymes that protect the PNS from the oxidative stress that results from fluctuations in blood glucose levels. This antioxidant ability may be involved in the mechanism by which Schwann cells are able to promote reconstruction in the CNS, especially in individuals with retinal injuries and degenerative diseases.

摘要

中枢神经系统(CNS)损伤后,除了髓鞘再生的情况外,再生通常不充分。CNS的这种髓鞘再生能力是干细胞/前体细胞介导的更新过程的一个很好的例子。雪旺细胞已被发现在外周神经系统(PNS)中作为髓鞘再生因子起作用,但多项研究也强调了它们在CNS髓鞘再生中的潜在作用。雪旺细胞能够通过分泌脑源性神经营养因子、胶质细胞系源性神经营养因子和碱性成纤维细胞生长因子等生长因子来保护和支持视网膜细胞。视网膜退行性疾病可能会使人极度虚弱,在老龄化国家是一个主要问题。西方导致永久性视力丧失的主要原因之一是一种称为年龄相关性黄斑变性(AMD)的视网膜退行性疾病。在美国,近175万40岁以上的人患有晚期AMD,据估计到2020年这个数字将增加到约300万人。视网膜疾病发生和发展过程中最常见的途径之一是氧化应激途径。在糖尿病患者中,雪旺细胞已被证明能够分泌大量抗氧化酶,保护PNS免受血糖水平波动所导致的氧化应激。这种抗氧化能力可能参与了雪旺细胞促进CNS重建的机制,尤其是在患有视网膜损伤和退行性疾病的个体中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2edf/5347187/48292dc367d3/mehdiophth-5-047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2edf/5347187/48292dc367d3/mehdiophth-5-047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2edf/5347187/48292dc367d3/mehdiophth-5-047-g001.jpg

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本文引用的文献

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Oxidative stress, inflamm-aging and immunosenescence.氧化应激、炎症性衰老和免疫衰老。
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