Cerebral ischemic damage in diabetes: an inflammatory perspective
Stroke is one of the leading causes of death worldwide. A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in i...
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Veröffentlicht in: | Journal of neuroinflammation 2017-01, Vol.14 (1), p.21-21, Article 21 |
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description | Stroke is one of the leading causes of death worldwide. A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in increased mortality and disabilities. Diabetes involves chronic inflammation manifested by reactive oxygen species generation, expression of proinflammatory cytokines, and activation/expression of other inflammatory mediators. It appears that increased proinflammatory processes due to diabetes are further accelerated after cerebral ischemia, leading to increased ischemic damage. Hypoglycemia is an intrinsic side effect owing to glucose-lowering therapy in diabetics, and is known to induce proinflammatory changes as well as exacerbate cerebral damage in experimental stroke. Here, we present a review of available literature on the contribution of neuroinflammation to increased cerebral ischemic damage in diabetics. We also describe the role of hypoglycemia in neuroinflammation and cerebral ischemic damage in diabetics. Understanding the role of neuroinflammatory mechanisms in worsening stroke outcome in diabetics may help limit ischemic brain injury and improve clinical outcomes. |
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A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in increased mortality and disabilities. Diabetes involves chronic inflammation manifested by reactive oxygen species generation, expression of proinflammatory cytokines, and activation/expression of other inflammatory mediators. It appears that increased proinflammatory processes due to diabetes are further accelerated after cerebral ischemia, leading to increased ischemic damage. Hypoglycemia is an intrinsic side effect owing to glucose-lowering therapy in diabetics, and is known to induce proinflammatory changes as well as exacerbate cerebral damage in experimental stroke. Here, we present a review of available literature on the contribution of neuroinflammation to increased cerebral ischemic damage in diabetics. We also describe the role of hypoglycemia in neuroinflammation and cerebral ischemic damage in diabetics. Understanding the role of neuroinflammatory mechanisms in worsening stroke outcome in diabetics may help limit ischemic brain injury and improve clinical outcomes.</description><identifier>ISSN: 1742-2094</identifier><identifier>EISSN: 1742-2094</identifier><identifier>DOI: 10.1186/s12974-016-0774-5</identifier><identifier>PMID: 28115020</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Brain - metabolism ; Brain damage ; Cerebral ischemia ; Cytokines - metabolism ; Diabetes Mellitus - physiopathology ; Diabetics ; Encephalitis - etiology ; Health aspects ; Humans ; Inflammation ; Review ; Stroke - complications ; Stroke - pathology</subject><ispartof>Journal of neuroinflammation, 2017-01, Vol.14 (1), p.21-21, Article 21</ispartof><rights>COPYRIGHT 2017 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-1d177c40a42c1c2f134ddbd3b11e678834580145d69aeda5dbb9bb8399e62d93</citedby><cites>FETCH-LOGICAL-c494t-1d177c40a42c1c2f134ddbd3b11e678834580145d69aeda5dbb9bb8399e62d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260103/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260103/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28115020$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shukla, Vibha</creatorcontrib><creatorcontrib>Shakya, Akhalesh Kumar</creatorcontrib><creatorcontrib>Perez-Pinzon, Miguel A</creatorcontrib><creatorcontrib>Dave, Kunjan R</creatorcontrib><title>Cerebral ischemic damage in diabetes: an inflammatory perspective</title><title>Journal of neuroinflammation</title><addtitle>J Neuroinflammation</addtitle><description>Stroke is one of the leading causes of death worldwide. A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in increased mortality and disabilities. Diabetes involves chronic inflammation manifested by reactive oxygen species generation, expression of proinflammatory cytokines, and activation/expression of other inflammatory mediators. It appears that increased proinflammatory processes due to diabetes are further accelerated after cerebral ischemia, leading to increased ischemic damage. Hypoglycemia is an intrinsic side effect owing to glucose-lowering therapy in diabetics, and is known to induce proinflammatory changes as well as exacerbate cerebral damage in experimental stroke. Here, we present a review of available literature on the contribution of neuroinflammation to increased cerebral ischemic damage in diabetics. We also describe the role of hypoglycemia in neuroinflammation and cerebral ischemic damage in diabetics. Understanding the role of neuroinflammatory mechanisms in worsening stroke outcome in diabetics may help limit ischemic brain injury and improve clinical outcomes.</description><subject>Animals</subject><subject>Brain - metabolism</subject><subject>Brain damage</subject><subject>Cerebral ischemia</subject><subject>Cytokines - metabolism</subject><subject>Diabetes Mellitus - physiopathology</subject><subject>Diabetics</subject><subject>Encephalitis - etiology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Review</subject><subject>Stroke - complications</subject><subject>Stroke - pathology</subject><issn>1742-2094</issn><issn>1742-2094</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNptUctO3DAUtSqq8mg_oBsUiQ2bUF-_krBAGo1KWwmpG_aWHzeDURIPdgaJv8fRUApV5YWv7XOO7z2HkK9ALwBa9S0D6xpRU1A1bUohP5AjaASrGe3EwZv6kBznfE8pZ1KxT-SQtQCSMnpEVmtMaJMZqpDdHY7BVd6MZoNVmCofjMUZ82VlpnLuBzOOZo7pqdpiylt0c3jEz-Rjb4aMX172E3J7_f12_bO--f3j13p1UzvRibkGD03jBDWCOXCsBy68t55bAFRN23IhWwpCetUZ9EZ6aztrW951qJjv-Am52stud3ZE73CaS9d6m8Jo0pOOJuj3L1O405v4qCVTFCgvAucvAik-7DDPeiwj4zCYCeMu62IoKNpKxgr07B_ofdylqUy3oIpxQknxF7UxA-piTyz_ukVUr0RLFZUclr4v_oMqyy9mxwn7UO7fEWBPcCnmnLB_nRGoXmLX-9h1iV0vsWtZOKdvzXll_MmZPwMkW6aY</recordid><startdate>20170123</startdate><enddate>20170123</enddate><creator>Shukla, Vibha</creator><creator>Shakya, Akhalesh Kumar</creator><creator>Perez-Pinzon, Miguel A</creator><creator>Dave, Kunjan R</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170123</creationdate><title>Cerebral ischemic damage in diabetes: an inflammatory perspective</title><author>Shukla, Vibha ; Shakya, Akhalesh Kumar ; Perez-Pinzon, Miguel A ; Dave, Kunjan R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-1d177c40a42c1c2f134ddbd3b11e678834580145d69aeda5dbb9bb8399e62d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Brain - metabolism</topic><topic>Brain damage</topic><topic>Cerebral ischemia</topic><topic>Cytokines - metabolism</topic><topic>Diabetes Mellitus - physiopathology</topic><topic>Diabetics</topic><topic>Encephalitis - etiology</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Review</topic><topic>Stroke - complications</topic><topic>Stroke - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shukla, Vibha</creatorcontrib><creatorcontrib>Shakya, Akhalesh Kumar</creatorcontrib><creatorcontrib>Perez-Pinzon, Miguel A</creatorcontrib><creatorcontrib>Dave, Kunjan R</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>Immunology Abstracts</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>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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuroinflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shukla, Vibha</au><au>Shakya, Akhalesh Kumar</au><au>Perez-Pinzon, Miguel A</au><au>Dave, Kunjan R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebral ischemic damage in diabetes: an inflammatory perspective</atitle><jtitle>Journal of neuroinflammation</jtitle><addtitle>J Neuroinflammation</addtitle><date>2017-01-23</date><risdate>2017</risdate><volume>14</volume><issue>1</issue><spage>21</spage><epage>21</epage><pages>21-21</pages><artnum>21</artnum><issn>1742-2094</issn><eissn>1742-2094</eissn><abstract>Stroke is one of the leading causes of death worldwide. A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in increased mortality and disabilities. Diabetes involves chronic inflammation manifested by reactive oxygen species generation, expression of proinflammatory cytokines, and activation/expression of other inflammatory mediators. It appears that increased proinflammatory processes due to diabetes are further accelerated after cerebral ischemia, leading to increased ischemic damage. Hypoglycemia is an intrinsic side effect owing to glucose-lowering therapy in diabetics, and is known to induce proinflammatory changes as well as exacerbate cerebral damage in experimental stroke. Here, we present a review of available literature on the contribution of neuroinflammation to increased cerebral ischemic damage in diabetics. 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subjects | Animals Brain - metabolism Brain damage Cerebral ischemia Cytokines - metabolism Diabetes Mellitus - physiopathology Diabetics Encephalitis - etiology Health aspects Humans Inflammation Review Stroke - complications Stroke - pathology |
title | Cerebral ischemic damage in diabetes: an inflammatory perspective |
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