Ischemic Preconditioning: A Novel Target for Neuroprotective Therapy
Ischemic preconditioning involves a brief exposure to ischemia in order to develop a tolerance to injurious effects of prolonged ischemia. The molecular mechanisms of neuroprotection that lead to ischemic tolerance are not yet completely understood. However, it seems that two distinct phases are inv...
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Veröffentlicht in: | Cerebrovascular diseases (Basel, Switzerland) Switzerland), 2006-05, Vol.21 (Suppl 2), p.38-47 |
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creator | Blanco, Miguel Lizasoain, Ignacio Sobrino, Tomás Vivancos, José Castillo, José |
description | Ischemic preconditioning involves a brief exposure to ischemia in order to develop a tolerance to injurious effects of prolonged ischemia. The molecular mechanisms of neuroprotection that lead to ischemic tolerance are not yet completely understood. However, it seems that two distinct phases are involved. Firstly, a cellular defense function against ischemia may be developed by the mechanisms inherent to neurons such as posttranslational modification of proteins or expression of new proteins via a signal transduction system to the nucleus. Secondly, a stress response and synthesis of stress proteins (heat shock proteins) may be activated. These mechanisms are mediated by chaperones. The objective of ischemic preconditioning research is to identify the underlying endogenous protective cellular receptors and signaling cascades, with the long-term goal of allowing therapeutic augmentation of the endogenous protective mechanisms in cerebral ischemia and possibly development of new neuroprotective strategies for ischemic stroke treatment. |
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The molecular mechanisms of neuroprotection that lead to ischemic tolerance are not yet completely understood. However, it seems that two distinct phases are involved. Firstly, a cellular defense function against ischemia may be developed by the mechanisms inherent to neurons such as posttranslational modification of proteins or expression of new proteins via a signal transduction system to the nucleus. Secondly, a stress response and synthesis of stress proteins (heat shock proteins) may be activated. These mechanisms are mediated by chaperones. The objective of ischemic preconditioning research is to identify the underlying endogenous protective cellular receptors and signaling cascades, with the long-term goal of allowing therapeutic augmentation of the endogenous protective mechanisms in cerebral ischemia and possibly development of new neuroprotective strategies for ischemic stroke treatment.</description><identifier>ISSN: 1015-9770</identifier><identifier>ISBN: 380558122X</identifier><identifier>ISBN: 9783805581226</identifier><identifier>EISSN: 1421-9786</identifier><identifier>EISBN: 3318013501</identifier><identifier>EISBN: 9783318013504</identifier><identifier>DOI: 10.1159/000091702</identifier><identifier>PMID: 16651813</identifier><language>eng</language><publisher>Basel, Switzerland: S. 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Karger AG, Basel</rights><rights>Copyright 2006 S. Karger AG, Basel.</rights><rights>Copyright (c) 2006 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c276t-e9f0ed2527b69744d979a1b7651b2e01930a2dedc353167460500e7fb65093603</citedby><cites>FETCH-LOGICAL-c276t-e9f0ed2527b69744d979a1b7651b2e01930a2dedc353167460500e7fb65093603</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16651813$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blanco, Miguel</creatorcontrib><creatorcontrib>Lizasoain, Ignacio</creatorcontrib><creatorcontrib>Sobrino, Tomás</creatorcontrib><creatorcontrib>Vivancos, José</creatorcontrib><creatorcontrib>Castillo, José</creatorcontrib><title>Ischemic Preconditioning: A Novel Target for Neuroprotective Therapy</title><title>Cerebrovascular diseases (Basel, Switzerland)</title><addtitle>Cerebrovasc Dis</addtitle><description>Ischemic preconditioning involves a brief exposure to ischemia in order to develop a tolerance to injurious effects of prolonged ischemia. 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Academic</collection><jtitle>Cerebrovascular diseases (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blanco, Miguel</au><au>Lizasoain, Ignacio</au><au>Sobrino, Tomás</au><au>Vivancos, José</au><au>Castillo, José</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemic Preconditioning: A Novel Target for Neuroprotective Therapy</atitle><jtitle>Cerebrovascular diseases (Basel, Switzerland)</jtitle><addtitle>Cerebrovasc Dis</addtitle><date>2006-05</date><risdate>2006</risdate><volume>21</volume><issue>Suppl 2</issue><spage>38</spage><epage>47</epage><pages>38-47</pages><issn>1015-9770</issn><eissn>1421-9786</eissn><isbn>380558122X</isbn><isbn>9783805581226</isbn><eisbn>3318013501</eisbn><eisbn>9783318013504</eisbn><abstract>Ischemic preconditioning involves a brief exposure to ischemia in order to develop a tolerance to injurious effects of prolonged ischemia. The molecular mechanisms of neuroprotection that lead to ischemic tolerance are not yet completely understood. However, it seems that two distinct phases are involved. Firstly, a cellular defense function against ischemia may be developed by the mechanisms inherent to neurons such as posttranslational modification of proteins or expression of new proteins via a signal transduction system to the nucleus. Secondly, a stress response and synthesis of stress proteins (heat shock proteins) may be activated. These mechanisms are mediated by chaperones. The objective of ischemic preconditioning research is to identify the underlying endogenous protective cellular receptors and signaling cascades, with the long-term goal of allowing therapeutic augmentation of the endogenous protective mechanisms in cerebral ischemia and possibly development of new neuroprotective strategies for ischemic stroke treatment.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>16651813</pmid><doi>10.1159/000091702</doi><tpages>10</tpages></addata></record> |
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subjects | Adenosine Triphosphate - metabolism alpha-Linolenic Acid - pharmacology alpha-Linolenic Acid - therapeutic use Animals Brain - blood supply Brain - drug effects Brain - metabolism Brain Ischemia - genetics Brain Ischemia - metabolism Brain Ischemia - therapy Clinical Trials as Topic Cytokines - metabolism Diazoxide - pharmacology Diazoxide - therapeutic use Drug Evaluation, Preclinical Gene Expression Regulation Genes, Immediate-Early Heat-Shock Proteins - genetics Heat-Shock Proteins - metabolism Humans Ischemic Preconditioning - methods Models, Animal Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Potassium Channels - metabolism Receptors, Glutamate - metabolism Stroke - genetics Stroke - metabolism Stroke - therapy |
title | Ischemic Preconditioning: A Novel Target for Neuroprotective Therapy |
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