CXC chemokines play a critical role in liver injury, recovery, and regeneration
Abstract Background Hepatic ischemia/reperfusion (I/R) injury is a principal consideration of trauma, resectional liver surgery, and transplantation. Despite improvements in supportive care, hepatic I/R injury continues to negatively impact patient outcomes because of significant tissue damage and o...
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| Veröffentlicht in: | The American journal of surgery 2009-09, Vol.198 (3), p.415-419 |
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| creator | Clarke, Callisia N., M.D Kuboki, Satoshi, M.D Tevar, Amit, M.D Lentsch, Alex B., Ph.D Edwards, Michael, M.D |
| description | Abstract Background Hepatic ischemia/reperfusion (I/R) injury is a principal consideration of trauma, resectional liver surgery, and transplantation. Despite improvements in supportive care, hepatic I/R injury continues to negatively impact patient outcomes because of significant tissue damage and organ dysfunction. CXC chemokines have been implicated as key mediators in the deleterious inflammatory cascade after hepatic I/R and also as important, beneficial regulators of liver recovery and regeneration. As such, their potential to mediate both beneficial and detrimental effects on hepatocytes makes them a key target for therapy. Herein, we provide a review of the inflammatory mechanisms of hepatic I/R injury, with a focus on the divergent functions of CXC chemokines in this response compared with other liver insults, and offer an explanation of this apparent paradox. Data sources MEDLINE and PubMed. Conclusions CXC chemokines are key mediators of both the inflammatory response to hepatic I/R as well as the recovery from this injury. Their contrasting functions in the regeneration of liver mass after an ischemic insult indicates that therapeutic manipulation of these mediator pathways should differ depending on the surgical milieu. |
| doi_str_mv | 10.1016/j.amjsurg.2009.01.025 |
| format | Article |
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Despite improvements in supportive care, hepatic I/R injury continues to negatively impact patient outcomes because of significant tissue damage and organ dysfunction. CXC chemokines have been implicated as key mediators in the deleterious inflammatory cascade after hepatic I/R and also as important, beneficial regulators of liver recovery and regeneration. As such, their potential to mediate both beneficial and detrimental effects on hepatocytes makes them a key target for therapy. Herein, we provide a review of the inflammatory mechanisms of hepatic I/R injury, with a focus on the divergent functions of CXC chemokines in this response compared with other liver insults, and offer an explanation of this apparent paradox. Data sources MEDLINE and PubMed. Conclusions CXC chemokines are key mediators of both the inflammatory response to hepatic I/R as well as the recovery from this injury. Their contrasting functions in the regeneration of liver mass after an ischemic insult indicates that therapeutic manipulation of these mediator pathways should differ depending on the surgical milieu.</description><identifier>ISSN: 0002-9610</identifier><identifier>EISSN: 1879-1883</identifier><identifier>DOI: 10.1016/j.amjsurg.2009.01.025</identifier><identifier>PMID: 19716886</identifier><identifier>CODEN: AJSUAB</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Angiogenesis ; Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cell cycle ; Chemokines ; Chemokines, CXC - metabolism ; Chemokines, CXC - physiology ; CXC chemokines ; Cytokines ; Endothelium ; General aspects ; Hepatocytes ; Humans ; Impact damage ; Inflammation ; Inflammation Mediators - metabolism ; Inflammation Mediators - physiology ; Inflammatory response ; Injuries ; Ischemia ; Ischemia - metabolism ; Ischemia - physiopathology ; Ischemia/Reperfusion ; Liver ; Liver regeneration ; Liver Regeneration - physiology ; Liver transplantation ; Medical sciences ; Neutrophils ; Recovery ; Recovery of Function - physiology ; Regeneration ; Regulators ; Reperfusion ; Reperfusion Injury - metabolism ; Reperfusion Injury - physiopathology ; Rodents ; Signal Transduction ; Surgery ; Transcription factors ; Transplantation ; Trauma ; Tumor necrosis factor-TNF</subject><ispartof>The American journal of surgery, 2009-09, Vol.198 (3), p.415-419</ispartof><rights>Elsevier Inc.</rights><rights>2009 Elsevier Inc.</rights><rights>2009 INIST-CNRS</rights><rights>Copyright Elsevier Limited Sep 1, 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c644t-336f992356a12ea329c469a266c226233812e15cc91e35ac7bf1ca6a92f488083</citedby><cites>FETCH-LOGICAL-c644t-336f992356a12ea329c469a266c226233812e15cc91e35ac7bf1ca6a92f488083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1924858982?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27929,27930,46000,64390,64392,64394,72474</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21911191$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19716886$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Clarke, Callisia N., M.D</creatorcontrib><creatorcontrib>Kuboki, Satoshi, M.D</creatorcontrib><creatorcontrib>Tevar, Amit, M.D</creatorcontrib><creatorcontrib>Lentsch, Alex B., Ph.D</creatorcontrib><creatorcontrib>Edwards, Michael, M.D</creatorcontrib><title>CXC chemokines play a critical role in liver injury, recovery, and regeneration</title><title>The American journal of surgery</title><addtitle>Am J Surg</addtitle><description>Abstract Background Hepatic ischemia/reperfusion (I/R) injury is a principal consideration of trauma, resectional liver surgery, and transplantation. Despite improvements in supportive care, hepatic I/R injury continues to negatively impact patient outcomes because of significant tissue damage and organ dysfunction. CXC chemokines have been implicated as key mediators in the deleterious inflammatory cascade after hepatic I/R and also as important, beneficial regulators of liver recovery and regeneration. As such, their potential to mediate both beneficial and detrimental effects on hepatocytes makes them a key target for therapy. Herein, we provide a review of the inflammatory mechanisms of hepatic I/R injury, with a focus on the divergent functions of CXC chemokines in this response compared with other liver insults, and offer an explanation of this apparent paradox. Data sources MEDLINE and PubMed. Conclusions CXC chemokines are key mediators of both the inflammatory response to hepatic I/R as well as the recovery from this injury. Their contrasting functions in the regeneration of liver mass after an ischemic insult indicates that therapeutic manipulation of these mediator pathways should differ depending on the surgical milieu.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cell cycle</subject><subject>Chemokines</subject><subject>Chemokines, CXC - metabolism</subject><subject>Chemokines, CXC - physiology</subject><subject>CXC chemokines</subject><subject>Cytokines</subject><subject>Endothelium</subject><subject>General aspects</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Impact damage</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammation Mediators - physiology</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - physiopathology</subject><subject>Ischemia/Reperfusion</subject><subject>Liver</subject><subject>Liver regeneration</subject><subject>Liver Regeneration - physiology</subject><subject>Liver transplantation</subject><subject>Medical sciences</subject><subject>Neutrophils</subject><subject>Recovery</subject><subject>Recovery of Function - physiology</subject><subject>Regeneration</subject><subject>Regulators</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Surgery</subject><subject>Transcription factors</subject><subject>Transplantation</subject><subject>Trauma</subject><subject>Tumor necrosis factor-TNF</subject><issn>0002-9610</issn><issn>1879-1883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkk1v1DAQhi0EokvhJ4AiITiR4LETx74UoRVfUqUeAImb5XonW6dZe7GTlfbf42ijFnrhYHnGfvxqxu8Q8hJoBRTE-74yuz5NcVsxSlVFoaKseURWIFtVgpT8MVlRSlmpBNAz8iylPqcANX9KzkC1IKQUK3K1_rUu7A3uwq3zmIr9YI6FKWx0o7NmKGIYsHC-GNwBYw76KR7fFRFtyHmOjN_kbIseoxld8M_Jk84MCV8s-zn5-fnTj_XX8vLqy7f1x8vSiroeS85FpxTjjTDA0HCmbC2UYUJYxgTjXOZjaKxVgLwxtr3uwBphFOtqKank5-TipLufrne4sejHaAa9j25n4lEH4_S_N97d6G04aNZyAQ3NAm8XgRh-T5hGvXPJ4jAYj2FKWrS5jKbhGXz9AOzDFH1uToNitWykkixTzYmyMaQUsbsrBaieDdO9XgzTs2Gags6G5Xev_u7j_tXiUAbeLIBJ2ZAuGm9duuMYKIC8MvfhxGH-9YPDqJN16C1uXHZr1Jvg_lvKxQMFOzg_T8EtHjHdd60T01R_n6drHi6qcsA4438Ap_TKvg</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Clarke, Callisia N., M.D</creator><creator>Kuboki, Satoshi, M.D</creator><creator>Tevar, Amit, M.D</creator><creator>Lentsch, Alex B., Ph.D</creator><creator>Edwards, Michael, M.D</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</scope><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>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090901</creationdate><title>CXC chemokines play a critical role in liver injury, recovery, and regeneration</title><author>Clarke, Callisia N., M.D ; Kuboki, Satoshi, M.D ; Tevar, Amit, M.D ; Lentsch, Alex B., Ph.D ; Edwards, Michael, M.D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c644t-336f992356a12ea329c469a266c226233812e15cc91e35ac7bf1ca6a92f488083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cell cycle</topic><topic>Chemokines</topic><topic>Chemokines, CXC - metabolism</topic><topic>Chemokines, CXC - physiology</topic><topic>CXC chemokines</topic><topic>Cytokines</topic><topic>Endothelium</topic><topic>General aspects</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Impact damage</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammation Mediators - physiology</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - physiopathology</topic><topic>Ischemia/Reperfusion</topic><topic>Liver</topic><topic>Liver regeneration</topic><topic>Liver Regeneration - physiology</topic><topic>Liver transplantation</topic><topic>Medical sciences</topic><topic>Neutrophils</topic><topic>Recovery</topic><topic>Recovery of Function - physiology</topic><topic>Regeneration</topic><topic>Regulators</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Surgery</topic><topic>Transcription factors</topic><topic>Transplantation</topic><topic>Trauma</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Clarke, Callisia N., M.D</creatorcontrib><creatorcontrib>Kuboki, Satoshi, M.D</creatorcontrib><creatorcontrib>Tevar, Amit, M.D</creatorcontrib><creatorcontrib>Lentsch, Alex B., Ph.D</creatorcontrib><creatorcontrib>Edwards, Michael, M.D</creatorcontrib><collection>Pascal-Francis</collection><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>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Clarke, Callisia N., M.D</au><au>Kuboki, Satoshi, M.D</au><au>Tevar, Amit, M.D</au><au>Lentsch, Alex B., Ph.D</au><au>Edwards, Michael, M.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXC chemokines play a critical role in liver injury, recovery, and regeneration</atitle><jtitle>The American journal of surgery</jtitle><addtitle>Am J Surg</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>198</volume><issue>3</issue><spage>415</spage><epage>419</epage><pages>415-419</pages><issn>0002-9610</issn><eissn>1879-1883</eissn><coden>AJSUAB</coden><abstract>Abstract Background Hepatic ischemia/reperfusion (I/R) injury is a principal consideration of trauma, resectional liver surgery, and transplantation. Despite improvements in supportive care, hepatic I/R injury continues to negatively impact patient outcomes because of significant tissue damage and organ dysfunction. CXC chemokines have been implicated as key mediators in the deleterious inflammatory cascade after hepatic I/R and also as important, beneficial regulators of liver recovery and regeneration. As such, their potential to mediate both beneficial and detrimental effects on hepatocytes makes them a key target for therapy. Herein, we provide a review of the inflammatory mechanisms of hepatic I/R injury, with a focus on the divergent functions of CXC chemokines in this response compared with other liver insults, and offer an explanation of this apparent paradox. Data sources MEDLINE and PubMed. Conclusions CXC chemokines are key mediators of both the inflammatory response to hepatic I/R as well as the recovery from this injury. Their contrasting functions in the regeneration of liver mass after an ischemic insult indicates that therapeutic manipulation of these mediator pathways should differ depending on the surgical milieu.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>19716886</pmid><doi>10.1016/j.amjsurg.2009.01.025</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Animals Biological and medical sciences Cardiology. Vascular system Cell cycle Chemokines Chemokines, CXC - metabolism Chemokines, CXC - physiology CXC chemokines Cytokines Endothelium General aspects Hepatocytes Humans Impact damage Inflammation Inflammation Mediators - metabolism Inflammation Mediators - physiology Inflammatory response Injuries Ischemia Ischemia - metabolism Ischemia - physiopathology Ischemia/Reperfusion Liver Liver regeneration Liver Regeneration - physiology Liver transplantation Medical sciences Neutrophils Recovery Recovery of Function - physiology Regeneration Regulators Reperfusion Reperfusion Injury - metabolism Reperfusion Injury - physiopathology Rodents Signal Transduction Surgery Transcription factors Transplantation Trauma Tumor necrosis factor-TNF |
| title | CXC chemokines play a critical role in liver injury, recovery, and regeneration |
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