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The Role of Mitochondrial and Endoplasmic Reticulum Reactive Oxygen Species Production in Models of Perinatal Brain Injury

Journal article
Authors Gagandeep Singh-Mallah
Syam Nair
Mats Sandberg
Carina Mallard
Henrik Hagberg
Published in Antioxidants & Redox Signaling
Volume 31
Issue 9
Pages 643-663
ISSN 1523-0864
Publication year 2019
Published at Institute of Neuroscience and Physiology
Institute of Biomedicine
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 643-663
Language en
Links dx.doi.org/10.1089/ars.2019.7779
Keywords reactive oxygen species, neonatal hypoxia-ischemia, mitochondria, endoplasmic reticulum, sirtuins, antioxidants, manganese superoxide-dismutase, nrf2-inducible antioxidant defense, hypoxic-ischemic injury, oxidative stress, nadph oxidase, hydrogen-peroxide, free-radicals, er stress, sirt3 deacetylates, electron-transport, Biochemistry & Molecular Biology, Endocrinology & Metabolism
Subject categories Endocrinology and Diabetes

Abstract

Recent Advances and Critical Issues: Mechanisms underlying ER stress-associated ROS production have been primarily elucidated using either non-neuronal cells or adult neurodegenerative experimental models. Findings from mature brain cannot be simply transferred to the immature brain. Therefore, age-specific studies investigating ER stress modulators may help investigate ER stress-associated ROS pathways in the immature brain. New therapeutics such as mitochondrial site-specific ROS inhibitors that selectively inhibit superoxide (O-2(center dot-))/hydrogen peroxide (H2O2) production are currently being developed. Future Directions: Because ER stress and oxidative stress accentuate each other, a combinatorial therapy utilizing both antioxidants and ER stress inhibitors may prove to be more protective against perinatal brain injury. Moreover, multiple relevant targets need to be identified for targeting ROS before they are formed. The role of organelle-specific ROS in brain repair needs investigation.

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