Oxidative Stress and Microglial Response in Retinitis Pigmentosa

An imbalance between the production of reactive oxygen species (ROS) and anti-oxidant capacity results in oxidative injury to cellular components and molecules, which in turn disturbs the homeostasis of cells and organs. Although retinitis pigmentosa (RP) is a hereditary disease, non-genetic biologi...

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Main Authors: Yusuke Murakami, Yusaku Nakabeppu, Koh-Hei Sonoda
Format: Article
Language:English
Published: MDPI AG 2020-09-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/21/19/7170
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spelling doaj-cbd02543b80645809e27dde0aef415a82020-11-25T03:31:09ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-09-01217170717010.3390/ijms21197170Oxidative Stress and Microglial Response in Retinitis PigmentosaYusuke Murakami0Yusaku Nakabeppu1Koh-Hei Sonoda2Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, JapanDivision of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, JapanDepartment of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, JapanAn imbalance between the production of reactive oxygen species (ROS) and anti-oxidant capacity results in oxidative injury to cellular components and molecules, which in turn disturbs the homeostasis of cells and organs. Although retinitis pigmentosa (RP) is a hereditary disease, non-genetic biological factors including oxidative stress also modulate or contribute to the disease progression. In animal models of RP, the degenerating retina exhibits marked oxidative damage in the nucleic acids, proteins, and lipids, and anti-oxidant treatments substantially suppress photoreceptor cell death and microgliosis. Although the mechanisms by which oxidative stress mediates retinal degeneration have not been fully elucidated, our group has shown that oxidative DNA damage and its defense system are key regulators of microglial activation and photoreceptor degeneration in RP. In this review, we summarize the current evidence regarding oxidative stress in animal models and patients with RP. The clinical efficacy of anti-oxidant treatments for RP has not been fully established. Nevertheless, elucidating key biological processes that underlie oxidative damage in RP will be pivotal to understanding the pathology and developing a potent anti-oxidant strategy that targets specific cell types or molecules under oxidative stress.https://www.mdpi.com/1422-0067/21/19/7170retinitis pigmentosaoxidative stressmicrogliaoxidative DNA damage
collection DOAJ
language English
format Article
sources DOAJ
author Yusuke Murakami
Yusaku Nakabeppu
Koh-Hei Sonoda
spellingShingle Yusuke Murakami
Yusaku Nakabeppu
Koh-Hei Sonoda
Oxidative Stress and Microglial Response in Retinitis Pigmentosa
International Journal of Molecular Sciences
retinitis pigmentosa
oxidative stress
microglia
oxidative DNA damage
author_facet Yusuke Murakami
Yusaku Nakabeppu
Koh-Hei Sonoda
author_sort Yusuke Murakami
title Oxidative Stress and Microglial Response in Retinitis Pigmentosa
title_short Oxidative Stress and Microglial Response in Retinitis Pigmentosa
title_full Oxidative Stress and Microglial Response in Retinitis Pigmentosa
title_fullStr Oxidative Stress and Microglial Response in Retinitis Pigmentosa
title_full_unstemmed Oxidative Stress and Microglial Response in Retinitis Pigmentosa
title_sort oxidative stress and microglial response in retinitis pigmentosa
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1661-6596
1422-0067
publishDate 2020-09-01
description An imbalance between the production of reactive oxygen species (ROS) and anti-oxidant capacity results in oxidative injury to cellular components and molecules, which in turn disturbs the homeostasis of cells and organs. Although retinitis pigmentosa (RP) is a hereditary disease, non-genetic biological factors including oxidative stress also modulate or contribute to the disease progression. In animal models of RP, the degenerating retina exhibits marked oxidative damage in the nucleic acids, proteins, and lipids, and anti-oxidant treatments substantially suppress photoreceptor cell death and microgliosis. Although the mechanisms by which oxidative stress mediates retinal degeneration have not been fully elucidated, our group has shown that oxidative DNA damage and its defense system are key regulators of microglial activation and photoreceptor degeneration in RP. In this review, we summarize the current evidence regarding oxidative stress in animal models and patients with RP. The clinical efficacy of anti-oxidant treatments for RP has not been fully established. Nevertheless, elucidating key biological processes that underlie oxidative damage in RP will be pivotal to understanding the pathology and developing a potent anti-oxidant strategy that targets specific cell types or molecules under oxidative stress.
topic retinitis pigmentosa
oxidative stress
microglia
oxidative DNA damage
url https://www.mdpi.com/1422-0067/21/19/7170
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