Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage

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 indu...

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Veröffentlicht in:Stroke and vascular neurology 2019-06, Vol.4 (2), p.93-95
Hauptverfasser: Wan, Jieru, Ren, Honglei, Wang, Jian
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Wang, Jian
description 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.
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Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. 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source BMJ Open Access Journals; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Alzheimer's disease
Animals
Apoptosis
Autophagy
Brain - drug effects
Brain - metabolism
Brain - pathology
Brain cancer
Brain damage
Brain research
Cerebral Hemorrhage - drug therapy
Cerebral Hemorrhage - metabolism
Cerebral Hemorrhage - pathology
Ferroptosis
Ferroptosis - drug effects
Hemorrhage
Humans
Inflammation
Iron
Iron - blood
Iron - metabolism
Iron Chelating Agents - therapeutic use
Lipid peroxidation
Lipid Peroxidation - drug effects
Lipids
Mitochondria
Oxidative Stress - drug effects
Review
Stroke
Toxicity
Traumatic brain injury
title Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage
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