Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets

Intracerebral hemorrhage (ICH) is a highly fatal disease with mortality rate of approximately 50%. Oxidative stress (OS) is a prominent cause of brain injury in ICH. Important sources of reactive oxygen species after hemorrhage are mitochondria dysfunction, degradated products of erythrocytes, excit...

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Autores principales: Zhang, Yan, Khan, Suliman, Liu, Yang, Wu, Guofeng, Yong, V. Wee, Xue, Mengzhou
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Immunology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959663/
https://www.ncbi.nlm.nih.gov/pubmed/35355999
http://dx.doi.org/10.3389/fimmu.2022.847246
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author Zhang, Yan
Khan, Suliman
Liu, Yang
Wu, Guofeng
Yong, V. Wee
Xue, Mengzhou
author_facet Zhang, Yan
Khan, Suliman
Liu, Yang
Wu, Guofeng
Yong, V. Wee
Xue, Mengzhou
author_sort Zhang, Yan
collection PubMed
description Intracerebral hemorrhage (ICH) is a highly fatal disease with mortality rate of approximately 50%. Oxidative stress (OS) is a prominent cause of brain injury in ICH. Important sources of reactive oxygen species after hemorrhage are mitochondria dysfunction, degradated products of erythrocytes, excitotoxic glutamate, activated microglia and infiltrated neutrophils. OS harms the central nervous system after ICH mainly through impacting inflammation, killing brain cells and exacerbating damage of the blood brain barrier. This review discusses the sources and the possible molecular mechanisms of OS in producing brain injury in ICH, and anti-OS strategies to ameliorate the devastation of ICH.
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spelling pubmed-89596632022-03-29 Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets Zhang, Yan Khan, Suliman Liu, Yang Wu, Guofeng Yong, V. Wee Xue, Mengzhou Front Immunol Immunology Intracerebral hemorrhage (ICH) is a highly fatal disease with mortality rate of approximately 50%. Oxidative stress (OS) is a prominent cause of brain injury in ICH. Important sources of reactive oxygen species after hemorrhage are mitochondria dysfunction, degradated products of erythrocytes, excitotoxic glutamate, activated microglia and infiltrated neutrophils. OS harms the central nervous system after ICH mainly through impacting inflammation, killing brain cells and exacerbating damage of the blood brain barrier. This review discusses the sources and the possible molecular mechanisms of OS in producing brain injury in ICH, and anti-OS strategies to ameliorate the devastation of ICH. Frontiers Media S.A. 2022-03-09 /pmc/articles/PMC8959663/ /pubmed/35355999 http://dx.doi.org/10.3389/fimmu.2022.847246 Text en Copyright © 2022 Zhang, Khan, Liu, Wu, Yong and Xue https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Zhang, Yan
Khan, Suliman
Liu, Yang
Wu, Guofeng
Yong, V. Wee
Xue, Mengzhou
Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets
title Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets
title_full Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets
title_fullStr Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets
title_full_unstemmed Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets
title_short Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets
title_sort oxidative stress following intracerebral hemorrhage: from molecular mechanisms to therapeutic targets
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959663/
https://www.ncbi.nlm.nih.gov/pubmed/35355999
http://dx.doi.org/10.3389/fimmu.2022.847246
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