Research progress on oxidative stress regulating different types of neuronal death caused by epileptic seizures
Clinical and experimental data hints that prolonged and repeated epileptic seizures can lead to molecular, biochemical, metabolic, and structural changes in the brain, a continuous process of chronic brain injury that ultimately leads to neuronal death. The histological characteristics of hippocampa...
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Veröffentlicht in: | Neurological sciences 2022-11, Vol.43 (11), p.6279-6298 |
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description | Clinical and experimental data hints that prolonged and repeated epileptic seizures can lead to molecular, biochemical, metabolic, and structural changes in the brain, a continuous process of chronic brain injury that ultimately leads to neuronal death. The histological characteristics of hippocampal structure determine its high sensitivity to excitotoxicity and present different types of neuronal death, including apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis. Hippocampal neuronal death promotes the progression of epileptogenesis, seizures, and epilepsy and is closely related to the impairment of cognitive function. Massive evidence indicates that oxidative stress plays a critical role in different forms of neuronal death induced by epileptic seizures. The brain is particularly vulnerable to damage caused by oxidative stress, and an increase in oxidative stress biomarkers was found in various epilepsy types. The purpose of this review is to elucidate the molecular mechanism of neuronal death and explore the moderating effect of oxidative stress on epileptic seizure-induced neuronal death patterns so as to find potential intervention targets for neuroprotective treatment after epileptic seizures. |
doi_str_mv | 10.1007/s10072-022-06302-6 |
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The histological characteristics of hippocampal structure determine its high sensitivity to excitotoxicity and present different types of neuronal death, including apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis. Hippocampal neuronal death promotes the progression of epileptogenesis, seizures, and epilepsy and is closely related to the impairment of cognitive function. Massive evidence indicates that oxidative stress plays a critical role in different forms of neuronal death induced by epileptic seizures. The brain is particularly vulnerable to damage caused by oxidative stress, and an increase in oxidative stress biomarkers was found in various epilepsy types. The purpose of this review is to elucidate the molecular mechanism of neuronal death and explore the moderating effect of oxidative stress on epileptic seizure-induced neuronal death patterns so as to find potential intervention targets for neuroprotective treatment after epileptic seizures.</description><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Brain injury</subject><subject>Cognitive ability</subject><subject>Convulsions & seizures</subject><subject>Death</subject><subject>Epilepsy</subject><subject>Excitotoxicity</subject><subject>Ferroptosis</subject><subject>Hippocampus</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Necroptosis</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Oxidative stress</subject><subject>Psychiatry</subject><subject>Pyroptosis</subject><subject>Review Article</subject><subject>Seizures</subject><issn>1590-1874</issn><issn>1590-3478</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kU1LxDAQhoMouK7-AU8BL16q-WiT9iiLX7AgiJ5Dmky7XbptTVJx_fVmtwuCBw8zE4bnfWHyInRJyQ0lRN76XWcJYbEEJywRR2hGs4IkPJX58eFNc5meojPv14QQmlI-Q_0reNDOrPDg-tqB97jvcP_VWB2aT8A-7HcO6rGNm67GtqkqcNAFHLYDRLzCHYyu73SLLeiwwkaPHiwutxiGpoUhNAZ7aL7HaHWOTirderg4zDl6f7h_Wzwly5fH58XdMjE8YyHhhc5TaSivJDMFS0uQnBLKJE2Bc8OJNDYnBQhubSwuIQNJS2ZtIaq8zPgcXU--8ayPEXxQm8YbaFvdQT96xURRSCKFIBG9-oOu-9HFcyIlWSFpzjMeKTZRxvXeO6jU4JqNdltFidr9vpoyUDEDtc9AiSjik8hHuKvB_Vr_o_oBydyKuQ</recordid><startdate>20221101</startdate><enddate>20221101</enddate><creator>Sun, Haogang</creator><creator>Li, Xinxin</creator><creator>Guo, Qi</creator><creator>Liu, Songyan</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0619-2755</orcidid></search><sort><creationdate>20221101</creationdate><title>Research progress on oxidative stress regulating different types of neuronal death caused by epileptic seizures</title><author>Sun, Haogang ; Li, Xinxin ; Guo, Qi ; Liu, Songyan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c352t-39a847c13f72c924be731012714e33c307cd809e63dd63d37e5e71b2dd96f8b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Brain injury</topic><topic>Cognitive ability</topic><topic>Convulsions & seizures</topic><topic>Death</topic><topic>Epilepsy</topic><topic>Excitotoxicity</topic><topic>Ferroptosis</topic><topic>Hippocampus</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Necroptosis</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neuroradiology</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Oxidative stress</topic><topic>Psychiatry</topic><topic>Pyroptosis</topic><topic>Review Article</topic><topic>Seizures</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Haogang</creatorcontrib><creatorcontrib>Li, Xinxin</creatorcontrib><creatorcontrib>Guo, Qi</creatorcontrib><creatorcontrib>Liu, Songyan</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</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 Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Haogang</au><au>Li, Xinxin</au><au>Guo, Qi</au><au>Liu, Songyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Research progress on oxidative stress regulating different types of neuronal death caused by epileptic seizures</atitle><jtitle>Neurological sciences</jtitle><stitle>Neurol Sci</stitle><date>2022-11-01</date><risdate>2022</risdate><volume>43</volume><issue>11</issue><spage>6279</spage><epage>6298</epage><pages>6279-6298</pages><issn>1590-1874</issn><eissn>1590-3478</eissn><abstract>Clinical and experimental data hints that prolonged and repeated epileptic seizures can lead to molecular, biochemical, metabolic, and structural changes in the brain, a continuous process of chronic brain injury that ultimately leads to neuronal death. 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subjects | Apoptosis Autophagy Brain injury Cognitive ability Convulsions & seizures Death Epilepsy Excitotoxicity Ferroptosis Hippocampus Medicine Medicine & Public Health Necroptosis Neurology Neuroprotection Neuroradiology Neurosciences Neurosurgery Oxidative stress Psychiatry Pyroptosis Review Article Seizures |
title | Research progress on oxidative stress regulating different types of neuronal death caused by epileptic seizures |
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