Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia
Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible target...
Gespeichert in:
| Veröffentlicht in: | Antioxidants & redox signaling 2003-10, Vol.5 (5), p.597-607 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 607 |
|---|---|
| container_issue | 5 |
| container_start_page | 597 |
| container_title | Antioxidants & redox signaling |
| container_volume | 5 |
| creator | Sugawara, Taku Chan, Pak H |
| description | Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke. |
| doi_str_mv | 10.1089/152308603770310266 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71304596</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71304596</sourcerecordid><originalsourceid>FETCH-LOGICAL-c365t-58ac0e297b3ec0cf6b29e20f256b482cd3c7c7d3931dafd402f9f474c51adc9e3</originalsourceid><addsrcrecordid>eNplkEtLBDEQhIMo7rr6BzxITt5GO8kkmTnK4gsEwcd5yCQdd2QeazIj7r83yy548NRNdVXRfIScM7hiUJTXTHIBhQKhNQgGXKkDMmdS6kxrpg63OxdZcuQzchLjJwBwxuCYzFguixRRc_L6gsaOzTfS4WfzgT0NxjXWtJGa3tG1GVdDUjE2kQ6e9jiFoTctdZgu1PgRA7UYsA5JbKJdYdeYU3LkUwOe7eeCvN_dvi0fsqfn-8flzVNmhZJjJgtjAXmpa4EWrFc1L5GD51LVecGtE1Zb7UQpmDPe5cB96XOdW8mMsyWKBbnc9a7D8DVhHKsuvYBta3ocplhpJiCXpUpGvjPaMMQY0Ffr0HQmbCoG1RZl9R9lCl3s26e6Q_cX2bMTvwbpb2s</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71304596</pqid></control><display><type>article</type><title>Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia</title><source>MEDLINE</source><source>Mary Ann Liebert Online</source><creator>Sugawara, Taku ; Chan, Pak H</creator><creatorcontrib>Sugawara, Taku ; Chan, Pak H</creatorcontrib><description>Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke.</description><identifier>ISSN: 1523-0864</identifier><identifier>EISSN: 1557-7716</identifier><identifier>DOI: 10.1089/152308603770310266</identifier><identifier>PMID: 14580316</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Apoptosis - physiology ; Brain Ischemia - metabolism ; Brain Ischemia - physiopathology ; Cell Death ; DNA-(Apurinic or Apyrimidinic Site) Lyase - physiology ; Glutathione Peroxidase - metabolism ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mitochondria - physiology ; Models, Biological ; Neurons - metabolism ; Nitric Oxide Synthase - metabolism ; Reactive Oxygen Species - metabolism ; Signal Transduction - physiology ; Superoxide Dismutase - metabolism</subject><ispartof>Antioxidants & redox signaling, 2003-10, Vol.5 (5), p.597-607</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-58ac0e297b3ec0cf6b29e20f256b482cd3c7c7d3931dafd402f9f474c51adc9e3</citedby><cites>FETCH-LOGICAL-c365t-58ac0e297b3ec0cf6b29e20f256b482cd3c7c7d3931dafd402f9f474c51adc9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3042,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14580316$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sugawara, Taku</creatorcontrib><creatorcontrib>Chan, Pak H</creatorcontrib><title>Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia</title><title>Antioxidants & redox signaling</title><addtitle>Antioxid Redox Signal</addtitle><description>Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke.</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - physiopathology</subject><subject>Cell Death</subject><subject>DNA-(Apurinic or Apyrimidinic Site) Lyase - physiology</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Mitochondria - physiology</subject><subject>Models, Biological</subject><subject>Neurons - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Superoxide Dismutase - metabolism</subject><issn>1523-0864</issn><issn>1557-7716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkEtLBDEQhIMo7rr6BzxITt5GO8kkmTnK4gsEwcd5yCQdd2QeazIj7r83yy548NRNdVXRfIScM7hiUJTXTHIBhQKhNQgGXKkDMmdS6kxrpg63OxdZcuQzchLjJwBwxuCYzFguixRRc_L6gsaOzTfS4WfzgT0NxjXWtJGa3tG1GVdDUjE2kQ6e9jiFoTctdZgu1PgRA7UYsA5JbKJdYdeYU3LkUwOe7eeCvN_dvi0fsqfn-8flzVNmhZJjJgtjAXmpa4EWrFc1L5GD51LVecGtE1Zb7UQpmDPe5cB96XOdW8mMsyWKBbnc9a7D8DVhHKsuvYBta3ocplhpJiCXpUpGvjPaMMQY0Ffr0HQmbCoG1RZl9R9lCl3s26e6Q_cX2bMTvwbpb2s</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Sugawara, Taku</creator><creator>Chan, Pak H</creator><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>7X8</scope></search><sort><creationdate>20031001</creationdate><title>Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia</title><author>Sugawara, Taku ; Chan, Pak H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-58ac0e297b3ec0cf6b29e20f256b482cd3c7c7d3931dafd402f9f474c51adc9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - physiopathology</topic><topic>Cell Death</topic><topic>DNA-(Apurinic or Apyrimidinic Site) Lyase - physiology</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Mitochondria - physiology</topic><topic>Models, Biological</topic><topic>Neurons - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - physiology</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sugawara, Taku</creatorcontrib><creatorcontrib>Chan, Pak H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Antioxidants & redox signaling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sugawara, Taku</au><au>Chan, Pak H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia</atitle><jtitle>Antioxidants & redox signaling</jtitle><addtitle>Antioxid Redox Signal</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>5</volume><issue>5</issue><spage>597</spage><epage>607</epage><pages>597-607</pages><issn>1523-0864</issn><eissn>1557-7716</eissn><abstract>Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke.</abstract><cop>United States</cop><pmid>14580316</pmid><doi>10.1089/152308603770310266</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1523-0864 |
| ispartof | Antioxidants & redox signaling, 2003-10, Vol.5 (5), p.597-607 |
| issn | 1523-0864 1557-7716 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71304596 |
| source | MEDLINE; Mary Ann Liebert Online |
| subjects | Animals Apoptosis - physiology Brain Ischemia - metabolism Brain Ischemia - physiopathology Cell Death DNA-(Apurinic or Apyrimidinic Site) Lyase - physiology Glutathione Peroxidase - metabolism Humans Mice Mice, Knockout Mice, Transgenic Mitochondria - physiology Models, Biological Neurons - metabolism Nitric Oxide Synthase - metabolism Reactive Oxygen Species - metabolism Signal Transduction - physiology Superoxide Dismutase - metabolism |
| title | Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T14%3A55%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Reactive%20oxygen%20radicals%20and%20pathogenesis%20of%20neuronal%20death%20after%20cerebral%20ischemia&rft.jtitle=Antioxidants%20&%20redox%20signaling&rft.au=Sugawara,%20Taku&rft.date=2003-10-01&rft.volume=5&rft.issue=5&rft.spage=597&rft.epage=607&rft.pages=597-607&rft.issn=1523-0864&rft.eissn=1557-7716&rft_id=info:doi/10.1089/152308603770310266&rft_dat=%3Cproquest_cross%3E71304596%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=71304596&rft_id=info:pmid/14580316&rfr_iscdi=true |