Plaminogen activator inhibitor-type 1: Its plasma determinants and relation with cardiovascular risk
article
The habitual level of PAI-1 is influenced by many factors, of which obesity and insulin resistance are the most important. It is possible to reduce plasma PAI-1 by changes in life style, e.g. weight reduction and physical activity. Data on potential interactions between environmental and metabolic variables on one hand, and the 4G/5G-polymorphism on the other hand, are still scarce. It becomes more and more clear that PAI-1 may possibly not be a major (causal) factor in cardiovascular disease, but its role in inflammation deserves further attention. In the presence of the 4G-allele not only the PAI-1 response was more pronounced, but also the response of other acute-phase reactants, which implies that the increases of these reactants are secondary to the increase in PAI-1. A myocardial infarction also provokes an acute phase response. It can thus be hypothesized that the 4G-allele might exacerbate tissue injury during the acute phase after a myocardial infarction, and thereby negatively affect the prognosis. © 2004 Schattauer GmbH, Stuttgart. Chemicals / CAS: alpha tocopherol, 1406-18-4, 1406-70-8, 52225-20-4, 58-95-7, 59-02-9; ascorbic acid, 134-03-2, 15421-15-5, 50-81-7; insulin, 9004-10-8; plasminogen activator inhibitor 1, 140208-23-7; tissue plasminogen activator, 105913-11-9; Plasminogen Activator Inhibitor 1
Topics
DeterminantsPAI-IReviewalpha tocopherolantioxidantascorbic aciddipeptidyl carboxypeptidase inhibitorinsulinlow density lipoproteinomega 3 fatty acidoral contraceptive agentplasminogen activator inhibitor 1tissue plasminogen activatortriacylglycerolacute phase responseallelecardiovascular diseasecardiovascular riskcircadian rhythmdisease exacerbationexercisegenetic polymorphismheart infarctionhypertensioninflammationinsulin resistanceischemic heart diseaselifestylenonhumanobesityphysical activityprognosisprotein blood levelprotein secretionrenin angiotensin aldosterone systemsmoking cessationstroketranscription regulationweight reductionbloodgeneticsphysiologyrisk factorCardiovascular DiseasesHumansPlasminogen Activator Inhibitor 1Polymorphism, GeneticRisk Factors
TNO Identifier
237750
ISSN
03406245
Source
Thrombosis and Haemostasis, 91(5), pp. 861-872.
Pages
861-872
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