Inflammation and plaque vulnerability
Atherosclerosis is a maladaptive, nonresolving chronic inflammatory disease that occurs at sites of blood flow disturbance. The disease usually remains silent until a breakdown of integrity at the arterial surface triggers the formation of a thrombus. By occluding the lumen, the thrombus or emboli d...
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| Veröffentlicht in: | Journal of internal medicine 2015-11, Vol.278 (5), p.483-493 |
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| container_title | Journal of internal medicine |
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| creator | Hansson, G. K. Libby, P. Tabas, I. |
| description | Atherosclerosis is a maladaptive, nonresolving chronic inflammatory disease that occurs at sites of blood flow disturbance. The disease usually remains silent until a breakdown of integrity at the arterial surface triggers the formation of a thrombus. By occluding the lumen, the thrombus or emboli detaching from it elicits ischaemic symptoms that may be life‐threatening. Two types of surface damage can cause atherothrombosis: plaque rupture and endothelial erosion. Plaque rupture is thought to be caused by loss of mechanical stability, often due to reduced tensile strength of the collagen cap surrounding the plaque. Therefore, plaques with reduced collagen content are thought to be more vulnerable than those with a thick collagen cap. Endothelial erosion, on the other hand, may occur after injurious insults to the endothelium instigated by metabolic disturbance or immune insults. This review discusses the molecular mechanisms involved in plaque vulnerability and the development of atherothrombosis. |
| doi_str_mv | 10.1111/joim.12406 |
| format | Article |
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K.</creatorcontrib><creatorcontrib>Libby, P.</creatorcontrib><creatorcontrib>Tabas, I.</creatorcontrib><title>Inflammation and plaque vulnerability</title><title>Journal of internal medicine</title><addtitle>J Intern Med</addtitle><description>Atherosclerosis is a maladaptive, nonresolving chronic inflammatory disease that occurs at sites of blood flow disturbance. The disease usually remains silent until a breakdown of integrity at the arterial surface triggers the formation of a thrombus. By occluding the lumen, the thrombus or emboli detaching from it elicits ischaemic symptoms that may be life‐threatening. Two types of surface damage can cause atherothrombosis: plaque rupture and endothelial erosion. Plaque rupture is thought to be caused by loss of mechanical stability, often due to reduced tensile strength of the collagen cap surrounding the plaque. Therefore, plaques with reduced collagen content are thought to be more vulnerable than those with a thick collagen cap. Endothelial erosion, on the other hand, may occur after injurious insults to the endothelium instigated by metabolic disturbance or immune insults. This review discusses the molecular mechanisms involved in plaque vulnerability and the development of atherothrombosis.</description><subject>Animals</subject><subject>atherosclerosis</subject><subject>atherothrombosis</subject><subject>Cysteine Proteases - metabolism</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>en‐dothelial erosion</subject><subject>Humans</subject><subject>inflammation</subject><subject>Inflammation - immunology</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Medicin och hälsovetenskap</subject><subject>plaque rupture</subject><subject>Plaque, Atherosclerotic - complications</subject><subject>Plaque, Atherosclerotic - pathology</subject><subject>Plaque, Atherosclerotic - physiopathology</subject><subject>Rupture, Spontaneous - complications</subject><subject>Rupture, Spontaneous - metabolism</subject><subject>Rupture, Spontaneous - physiopathology</subject><subject>Thromboembolism - etiology</subject><issn>0954-6820</issn><issn>1365-2796</issn><issn>1365-2796</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNp9kUFP2zAYhq1paHSMCz8A9TIJTQp8tmPHvkxCiG1FRVzG2fqafAEXJylxS9V_P5cUNg7MF1v28z62_DJ2xOGUp3E273xzykUO-gMbcalVJgqrP7IRWJVn2gjYZ59jnANwCRo-sX2hhQYJxYh9nbR1wKbBpe_aMbbVeBHwcUXjp1VoqceZD365-cL2agyRDnfzAbv9cfn74lc2vfk5uTifZqU2Smczqo0xWs2oAKmwIm7RSm0qoykvC4E2B0DEWgslSBlFFcoScpswFLqWBywbvHFNi9XMLXrfYL9xHXq323pIK3KK8zyXibfv8ou-q_6GXoJcCqG0VUXKfh-yCWioKqld9hjeKt6ctP7e3XVPToER6duT4GQn6Lv0Y3HpGh9LCgFb6lbR8ULkQlkQIqHfBrTsuxh7ql-v4eC2Hbpth-65wwQf__uwV_SltATwAVj7QJv_qNzVzeR6kP4BjCqoog</recordid><startdate>201511</startdate><enddate>201511</enddate><creator>Hansson, G. K.</creator><creator>Libby, P.</creator><creator>Tabas, I.</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><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>201511</creationdate><title>Inflammation and plaque vulnerability</title><author>Hansson, G. K. ; Libby, P. ; Tabas, I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6856-bef88865be7035ade19a9368d86e4c72a9400aaaf6252e585eda3c0499a9a26f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>atherosclerosis</topic><topic>atherothrombosis</topic><topic>Cysteine Proteases - metabolism</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>en‐dothelial erosion</topic><topic>Humans</topic><topic>inflammation</topic><topic>Inflammation - immunology</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Medicin och hälsovetenskap</topic><topic>plaque rupture</topic><topic>Plaque, Atherosclerotic - complications</topic><topic>Plaque, Atherosclerotic - pathology</topic><topic>Plaque, Atherosclerotic - physiopathology</topic><topic>Rupture, Spontaneous - complications</topic><topic>Rupture, Spontaneous - metabolism</topic><topic>Rupture, Spontaneous - physiopathology</topic><topic>Thromboembolism - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hansson, G. K.</creatorcontrib><creatorcontrib>Libby, P.</creatorcontrib><creatorcontrib>Tabas, I.</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><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>Journal of internal medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hansson, G. 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| ispartof | Journal of internal medicine, 2015-11, Vol.278 (5), p.483-493 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SWEPUB Freely available online; Wiley Free Content; Wiley Online Library All Journals |
| subjects | Animals atherosclerosis atherothrombosis Cysteine Proteases - metabolism Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Endothelium, Vascular - physiopathology en‐dothelial erosion Humans inflammation Inflammation - immunology Matrix Metalloproteinases - metabolism Medicin och hälsovetenskap plaque rupture Plaque, Atherosclerotic - complications Plaque, Atherosclerotic - pathology Plaque, Atherosclerotic - physiopathology Rupture, Spontaneous - complications Rupture, Spontaneous - metabolism Rupture, Spontaneous - physiopathology Thromboembolism - etiology |
| title | Inflammation and plaque vulnerability |
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