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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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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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.</description><identifier>ISSN: 2059-8688</identifier><identifier>EISSN: 2059-8696</identifier><identifier>DOI: 10.1136/svn-2018-000205</identifier><identifier>PMID: 31338218</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>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</subject><ispartof>Stroke and vascular neurology, 2019-06, Vol.4 (2), p.93-95</ispartof><rights>2019 Author(s) (or their employer(s)) 2019. 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. Published by BMJ. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-154e8f5e62ad12140cd2fc963684934ef4f3f078f194f4008d4d75d8dc8f9ef3</citedby><cites>FETCH-LOGICAL-c421t-154e8f5e62ad12140cd2fc963684934ef4f3f078f194f4008d4d75d8dc8f9ef3</cites><orcidid>0000-0003-2291-640X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613877/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613877/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31338218$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wan, Jieru</creatorcontrib><creatorcontrib>Ren, Honglei</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><title>Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage</title><title>Stroke and vascular neurology</title><addtitle>Stroke Vasc Neurol</addtitle><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.</description><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain cancer</subject><subject>Brain damage</subject><subject>Brain research</subject><subject>Cerebral Hemorrhage - drug therapy</subject><subject>Cerebral Hemorrhage - metabolism</subject><subject>Cerebral Hemorrhage - pathology</subject><subject>Ferroptosis</subject><subject>Ferroptosis - drug effects</subject><subject>Hemorrhage</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Iron</subject><subject>Iron - blood</subject><subject>Iron - metabolism</subject><subject>Iron Chelating Agents - therapeutic use</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Lipids</subject><subject>Mitochondria</subject><subject>Oxidative Stress - drug effects</subject><subject>Review</subject><subject>Stroke</subject><subject>Toxicity</subject><subject>Traumatic brain injury</subject><issn>2059-8688</issn><issn>2059-8696</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkUtLAzEURoMotlTX7mTAjQtH85o0sxGk-CgIIrgPaXLTRqaTMZmK_femtBZ1k4Tck497cxA6I_iaECZu0mdbUkxkiTGmuDpAw7zWpRS1ONyfpRyg05TeM0PkeFzj-hgNGGFMUiKH6HUaQ1v04csb36-visZ33hYdxHxjde9zUbe2cBBj6PqQfCq06yEWvu2jNhBhFnVTLDQsQ4wLPYcTdOR0k-B0t4_Q28P92-SpfH55nE7unkvDKelLUnGQrgJBtSWUcGwsdaYWTEheMw6OO-bwWDpSc8cxlpbbcWWlNdLV4NgI3W5ju9VsCdbApp9GddEvdVyroL36W2n9Qs3DpxKCsPwROeByFxDDxwpSr5Y-GWga3UJYJUWpYIwySnlGL_6h72EV2zydolXFNjIkzdTNljIxpBTB7ZshWG0YlYWpjTC1FZZfnP-eYc__6GHfs6SS2Q</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>Wan, Jieru</creator><creator>Ren, Honglei</creator><creator>Wang, Jian</creator><general>BMJ Publishing Group LTD</general><general>BMJ Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2291-640X</orcidid></search><sort><creationdate>20190601</creationdate><title>Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage</title><author>Wan, Jieru ; Ren, Honglei ; Wang, Jian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-154e8f5e62ad12140cd2fc963684934ef4f3f078f194f4008d4d75d8dc8f9ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain cancer</topic><topic>Brain damage</topic><topic>Brain research</topic><topic>Cerebral Hemorrhage - drug therapy</topic><topic>Cerebral Hemorrhage - metabolism</topic><topic>Cerebral Hemorrhage - pathology</topic><topic>Ferroptosis</topic><topic>Ferroptosis - drug effects</topic><topic>Hemorrhage</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Iron</topic><topic>Iron - blood</topic><topic>Iron - metabolism</topic><topic>Iron Chelating Agents - therapeutic use</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Lipids</topic><topic>Mitochondria</topic><topic>Oxidative Stress - drug effects</topic><topic>Review</topic><topic>Stroke</topic><topic>Toxicity</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wan, Jieru</creatorcontrib><creatorcontrib>Ren, Honglei</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Stroke and vascular neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wan, Jieru</au><au>Ren, Honglei</au><au>Wang, Jian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage</atitle><jtitle>Stroke and vascular neurology</jtitle><addtitle>Stroke Vasc Neurol</addtitle><date>2019-06-01</date><risdate>2019</risdate><volume>4</volume><issue>2</issue><spage>93</spage><epage>95</epage><pages>93-95</pages><issn>2059-8688</issn><eissn>2059-8696</eissn><abstract>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.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>31338218</pmid><doi>10.1136/svn-2018-000205</doi><tpages>3</tpages><orcidid>https://orcid.org/0000-0003-2291-640X</orcidid><oa>free_for_read</oa></addata></record> |
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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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