Inflammatory role of platelets in acute coronary syndromes
[...]CD40L stimulation increases the expression of adhesion molecules, chemokines, and inflammatory cytokines leading to recruitment and activation of leucocytes within the plaque. 4 14 Secondly, both soluble and membrane bound CD40L are potent inducers and activators of MMPs in macrophages and vasc...
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| Veröffentlicht in: | British heart journal 2001-12, Vol.86 (6), p.605-606 |
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| creator | AUKRUST, PÅL WÆHRE, TORGUN DAMÅS, JAN KRISTIN GULLESTAD, LARS SOLUM, NILS OLAV |
| description | [...]CD40L stimulation increases the expression of adhesion molecules, chemokines, and inflammatory cytokines leading to recruitment and activation of leucocytes within the plaque. 4 14 Secondly, both soluble and membrane bound CD40L are potent inducers and activators of MMPs in macrophages and vascular SMC, 14 and such activation may play a crucial role in undermining the integrity of tissue components in an atherosclerotic plaque. 1 2 Finally, CD40-CD40L interaction may promote thrombotic activity by enhancing tissue factor expression in macrophages and through direct regulation of endothelium associated procoagulant activity. 14 Consequently, in acute coronary syndromes activated platelets may, by providing CD40L, contribute to inflammatory reactions, MMP activation, and procoagulant activity within an atherosclerotic plaque. |
| doi_str_mv | 10.1136/heart.86.6.605 |
| format | Article |
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Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>AUKRUST, PÅL ; WÆHRE, TORGUN ; DAMÅS, JAN KRISTIN ; GULLESTAD, LARS ; SOLUM, NILS OLAV</creator><creatorcontrib>AUKRUST, PÅL ; WÆHRE, TORGUN ; DAMÅS, JAN KRISTIN ; GULLESTAD, LARS ; SOLUM, NILS OLAV</creatorcontrib><description>[...]CD40L stimulation increases the expression of adhesion molecules, chemokines, and inflammatory cytokines leading to recruitment and activation of leucocytes within the plaque. 4 14 Secondly, both soluble and membrane bound CD40L are potent inducers and activators of MMPs in macrophages and vascular SMC, 14 and such activation may play a crucial role in undermining the integrity of tissue components in an atherosclerotic plaque. 1 2 Finally, CD40-CD40L interaction may promote thrombotic activity by enhancing tissue factor expression in macrophages and through direct regulation of endothelium associated procoagulant activity. 14 Consequently, in acute coronary syndromes activated platelets may, by providing CD40L, contribute to inflammatory reactions, MMP activation, and procoagulant activity within an atherosclerotic plaque.</description><identifier>ISSN: 1355-6037</identifier><identifier>ISSN: 0007-0769</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/heart.86.6.605</identifier><identifier>PMID: 11711447</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>Acute coronary syndromes ; Acute Disease ; Adhesion ; Angina pectoris ; Apoptosis ; Blood clots ; Blood platelets ; Blood Platelets - physiology ; Cardiovascular disease ; Causes of ; CD40 Antigens - metabolism ; CD40 Ligand - metabolism ; Chemokines ; Coronary Disease - blood ; Coronary Disease - pathology ; Cytokines ; Endothelium ; Heart attack ; Heart attacks ; Humans ; Inflammation ; Inflammation - blood ; Inflammation - immunology ; Leukocytes ; Ligands ; Mediators ; Pathogenesis ; Physiological aspects ; Platelet Aggregation Inhibitors - therapeutic use ; Rodents ; Studies ; Syndrome ; Tumor necrosis factor-TNF ; Unstable angina</subject><ispartof>British heart journal, 2001-12, Vol.86 (6), p.605-606</ispartof><rights>British Cardiac Society</rights><rights>COPYRIGHT 2001 BMJ Publishing Group Ltd.</rights><rights>Copyright: 2001 British Cardiac Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b627t-cb068859a0c60296ff97c2da03acc1b885728b4a0f56567d80d96c8e662aa0d03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1730032/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1730032/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11711447$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AUKRUST, PÅL</creatorcontrib><creatorcontrib>WÆHRE, TORGUN</creatorcontrib><creatorcontrib>DAMÅS, JAN KRISTIN</creatorcontrib><creatorcontrib>GULLESTAD, LARS</creatorcontrib><creatorcontrib>SOLUM, NILS OLAV</creatorcontrib><title>Inflammatory role of platelets in acute coronary syndromes</title><title>British heart journal</title><addtitle>Heart</addtitle><description>[...]CD40L stimulation increases the expression of adhesion molecules, chemokines, and inflammatory cytokines leading to recruitment and activation of leucocytes within the plaque. 4 14 Secondly, both soluble and membrane bound CD40L are potent inducers and activators of MMPs in macrophages and vascular SMC, 14 and such activation may play a crucial role in undermining the integrity of tissue components in an atherosclerotic plaque. 1 2 Finally, CD40-CD40L interaction may promote thrombotic activity by enhancing tissue factor expression in macrophages and through direct regulation of endothelium associated procoagulant activity. 14 Consequently, in acute coronary syndromes activated platelets may, by providing CD40L, contribute to inflammatory reactions, MMP activation, and procoagulant activity within an atherosclerotic plaque.</description><subject>Acute coronary syndromes</subject><subject>Acute Disease</subject><subject>Adhesion</subject><subject>Angina pectoris</subject><subject>Apoptosis</subject><subject>Blood clots</subject><subject>Blood platelets</subject><subject>Blood Platelets - physiology</subject><subject>Cardiovascular disease</subject><subject>Causes of</subject><subject>CD40 Antigens - metabolism</subject><subject>CD40 Ligand - metabolism</subject><subject>Chemokines</subject><subject>Coronary Disease - blood</subject><subject>Coronary Disease - pathology</subject><subject>Cytokines</subject><subject>Endothelium</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - immunology</subject><subject>Leukocytes</subject><subject>Ligands</subject><subject>Mediators</subject><subject>Pathogenesis</subject><subject>Physiological aspects</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Rodents</subject><subject>Studies</subject><subject>Syndrome</subject><subject>Tumor necrosis factor-TNF</subject><subject>Unstable angina</subject><issn>1355-6037</issn><issn>0007-0769</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkd9rFDEQxxdRbK2--igLgiC45yTZTbI-COXwR8upIP7oW8hmZ697ZpMzyYr97029o1UpyDwkZD7z_c5kiuIhgQUhjD8_Rx3SQvJFDmhuFYek5rKiQM5u5ztrmooDEwfFvRg3AFC3kt8tDggRhNS1OCxenLjB6mnSyYeLMniLpR_KrdUJLaZYjq7UZk5YGh-805mJF64PfsJ4v7gzaBvxwf48Kj6_fvVp-bZafXhzsjxeVR2nIlWmAy5l02owHGjLh6EVhvYamDaGdDklqOxqDUPDGy56CX3LjUTOqdbQAzsqXu50t3M3YW_QpaCt2oZxyv0or0f1d8aN52rtfygiGACjWeDJXiD47zPGpKYxGrRWO_RzVIJSyVrgGXz8D7jxc3B5uKwlQbS0ZTJTz3bUWltUoxt8djVrdJjNvcNhzM_HkpBcQC7dqxvwHD1Oo7mJX-x4E3yMAYerSQmoy52r3ztXkqsc0OSCR3_-zzW-X_J1B2NM-PMqr8M3xQUTjXr_ZanOTr-u3p0yUB8z_3THd9Pmf-a_AJ03xPY</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>AUKRUST, PÅL</creator><creator>WÆHRE, TORGUN</creator><creator>DAMÅS, JAN KRISTIN</creator><creator>GULLESTAD, LARS</creator><creator>SOLUM, NILS OLAV</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</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>20011201</creationdate><title>Inflammatory role of platelets in acute coronary syndromes</title><author>AUKRUST, PÅL ; WÆHRE, TORGUN ; DAMÅS, JAN KRISTIN ; GULLESTAD, LARS ; SOLUM, NILS OLAV</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b627t-cb068859a0c60296ff97c2da03acc1b885728b4a0f56567d80d96c8e662aa0d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acute coronary syndromes</topic><topic>Acute Disease</topic><topic>Adhesion</topic><topic>Angina pectoris</topic><topic>Apoptosis</topic><topic>Blood clots</topic><topic>Blood platelets</topic><topic>Blood Platelets - physiology</topic><topic>Cardiovascular disease</topic><topic>Causes of</topic><topic>CD40 Antigens - metabolism</topic><topic>CD40 Ligand - metabolism</topic><topic>Chemokines</topic><topic>Coronary Disease - blood</topic><topic>Coronary Disease - pathology</topic><topic>Cytokines</topic><topic>Endothelium</topic><topic>Heart attack</topic><topic>Heart attacks</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - immunology</topic><topic>Leukocytes</topic><topic>Ligands</topic><topic>Mediators</topic><topic>Pathogenesis</topic><topic>Physiological aspects</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Rodents</topic><topic>Studies</topic><topic>Syndrome</topic><topic>Tumor necrosis factor-TNF</topic><topic>Unstable angina</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AUKRUST, PÅL</creatorcontrib><creatorcontrib>WÆHRE, TORGUN</creatorcontrib><creatorcontrib>DAMÅS, JAN KRISTIN</creatorcontrib><creatorcontrib>GULLESTAD, LARS</creatorcontrib><creatorcontrib>SOLUM, NILS OLAV</creatorcontrib><collection>Istex</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</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>BMJ Journals</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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>British heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AUKRUST, PÅL</au><au>WÆHRE, TORGUN</au><au>DAMÅS, JAN KRISTIN</au><au>GULLESTAD, LARS</au><au>SOLUM, NILS OLAV</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammatory role of platelets in acute coronary syndromes</atitle><jtitle>British heart journal</jtitle><addtitle>Heart</addtitle><date>2001-12-01</date><risdate>2001</risdate><volume>86</volume><issue>6</issue><spage>605</spage><epage>606</epage><pages>605-606</pages><issn>1355-6037</issn><issn>0007-0769</issn><eissn>1468-201X</eissn><abstract>[...]CD40L stimulation increases the expression of adhesion molecules, chemokines, and inflammatory cytokines leading to recruitment and activation of leucocytes within the plaque. 4 14 Secondly, both soluble and membrane bound CD40L are potent inducers and activators of MMPs in macrophages and vascular SMC, 14 and such activation may play a crucial role in undermining the integrity of tissue components in an atherosclerotic plaque. 1 2 Finally, CD40-CD40L interaction may promote thrombotic activity by enhancing tissue factor expression in macrophages and through direct regulation of endothelium associated procoagulant activity. 14 Consequently, in acute coronary syndromes activated platelets may, by providing CD40L, contribute to inflammatory reactions, MMP activation, and procoagulant activity within an atherosclerotic plaque.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>11711447</pmid><doi>10.1136/heart.86.6.605</doi><tpages>2</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Acute coronary syndromes Acute Disease Adhesion Angina pectoris Apoptosis Blood clots Blood platelets Blood Platelets - physiology Cardiovascular disease Causes of CD40 Antigens - metabolism CD40 Ligand - metabolism Chemokines Coronary Disease - blood Coronary Disease - pathology Cytokines Endothelium Heart attack Heart attacks Humans Inflammation Inflammation - blood Inflammation - immunology Leukocytes Ligands Mediators Pathogenesis Physiological aspects Platelet Aggregation Inhibitors - therapeutic use Rodents Studies Syndrome Tumor necrosis factor-TNF Unstable angina |
| title | Inflammatory role of platelets in acute coronary syndromes |
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