author_facet Wan, Jieru
Ren, Honglei
Wang, Jian
Wan, Jieru
Ren, Honglei
Wang, Jian
author Wan, Jieru
Ren, Honglei
Wang, Jian
spellingShingle Wan, Jieru
Ren, Honglei
Wang, Jian
Stroke and Vascular Neurology
Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
Cardiology and Cardiovascular Medicine
Neurology (clinical)
author_sort wan, jieru
spelling Wan, Jieru Ren, Honglei Wang, Jian 2059-8688 2059-8696 BMJ Cardiology and Cardiovascular Medicine Neurology (clinical) http://dx.doi.org/10.1136/svn-2018-000205 <jats:p>Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention.</jats:p> Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage Stroke and Vascular Neurology
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title Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_unstemmed Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_full Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_fullStr Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_full_unstemmed Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_short Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_sort iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
topic Cardiology and Cardiovascular Medicine
Neurology (clinical)
url http://dx.doi.org/10.1136/svn-2018-000205
publishDate 2019
physical 93-95
description <jats:p>Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention.</jats:p>
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author Wan, Jieru, Ren, Honglei, Wang, Jian
author_facet Wan, Jieru, Ren, Honglei, Wang, Jian, Wan, Jieru, Ren, Honglei, Wang, Jian
author_sort wan, jieru
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description <jats:p>Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention.</jats:p>
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spelling Wan, Jieru Ren, Honglei Wang, Jian 2059-8688 2059-8696 BMJ Cardiology and Cardiovascular Medicine Neurology (clinical) http://dx.doi.org/10.1136/svn-2018-000205 <jats:p>Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention.</jats:p> Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage Stroke and Vascular Neurology
spellingShingle Wan, Jieru, Ren, Honglei, Wang, Jian, Stroke and Vascular Neurology, Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage, Cardiology and Cardiovascular Medicine, Neurology (clinical)
title Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_full Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_fullStr Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_full_unstemmed Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_short Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_sort iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
title_unstemmed Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
topic Cardiology and Cardiovascular Medicine, Neurology (clinical)
url http://dx.doi.org/10.1136/svn-2018-000205