Fibrinogen and fibrin clot structure in diabetes
Diabetes is associated with an increased risk of developing cardiovascular disease, which is not fully accounted for by the accumulation of classic cardiovascular risk factors in patients. Recent evidence has demonstrated fibrinogen to be a powerful independent risk marker for cardiovascular disease...
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Veröffentlicht in: | Herz 2004-08, Vol.29 (5), p.470-479 |
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description | Diabetes is associated with an increased risk of developing cardiovascular disease, which is not fully accounted for by the accumulation of classic cardiovascular risk factors in patients. Recent evidence has demonstrated fibrinogen to be a powerful independent risk marker for cardiovascular disease in the general population, and it is also likely to contribute toward the increased atherosclerotic risk in diabetes. The etiology of hyperfibrinogenemia in diabetes is likely to be multifactorial, and at present the mechanisms involved have not been clarified. However, insulin, insulin resistance and inflammation are likely to be involved, especially in type 2 diabetes. The influence of diabetes in determining an individual's atherothrombotic risk is likely to extend beyond that of elevated fibrinogen levels, and may also act via changes in the structure and function of the fibrin clot that forms. Further research is needed to determine the mechanisms underlying these changes, which may lead to development of future interventions to reduce the excessive vascular risk associated with this disease. |
doi_str_mv | 10.1007/s00059-004-2607-z |
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Further research is needed to determine the mechanisms underlying these changes, which may lead to development of future interventions to reduce the excessive vascular risk associated with this disease.</description><subject>Animals</subject><subject>Blood Coagulation - immunology</subject><subject>Diabetes Mellitus - immunology</subject><subject>Diabetic Angiopathies - immunology</subject><subject>Fibrin - immunology</subject><subject>Fibrinogen - immunology</subject><subject>Humans</subject><subject>Models, Immunological</subject><subject>Signal Transduction - immunology</subject><issn>0340-9937</issn><issn>1615-6692</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkD1PwzAQhi0EoqXwA1hQxMBmONvx14gqCkiVWGC2HMdGqdKk2MlAfz0ujYTEdF_vvXd6ELomcE8A5EMCAK4xQImpAIn3J2hOBOFYCE1P0RxYCVhrJmfoIqUNAOGawjmaEZ4nktE5glVTxabrP31X2K4uwm9ZuLYfijTE0Q1j9EXu1I2t_ODTJToLtk3-aooL9LF6el--4PXb8-vycY0do-WAiWCChpooHZTNqZcKGLfaMmYrpSQHJ4ISXHpRUpHbtSOldjYoVpEQKrZAd0ffXey_Rp8Gs22S821rO9-PyQihGOdQZuHtP-GmH2OXfzMU8h3C9EFEjiIX-5SiD2YXm62N34aAObA0R5YmszQHlmafd24m47Ha-vpvY4LHfgAoIm13</recordid><startdate>200408</startdate><enddate>200408</enddate><creator>Dunn, Emma J</creator><creator>Ariëns, Robert A S</creator><general>Springer Nature B.V</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>7TS</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200408</creationdate><title>Fibrinogen and fibrin clot structure in diabetes</title><author>Dunn, Emma J ; 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subjects | Animals Blood Coagulation - immunology Diabetes Mellitus - immunology Diabetic Angiopathies - immunology Fibrin - immunology Fibrinogen - immunology Humans Models, Immunological Signal Transduction - immunology |
title | Fibrinogen and fibrin clot structure in diabetes |
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