IMR Press / FBS / Volume 2 / Issue 1 / DOI: 10.2741/S57

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Pathophysiology of the proatherothrombotic state in the metabolic syndrome
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1 Research Program of Cardiovascular Disease Risk, Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Universidad de Talca, Chile
2 Biomedical Research Laboratory, School of Medicine, Universidad Catolica del Maule, Chile
3 Research Center, Hospital Universitario La Fe, Valencia, Spain
4 Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Cientificas, Valencia, Spain

*Author to whom correspondence should be addressed.


Front. Biosci. (Schol Ed) 2010, 2(1), 194–208;
Published: 1 January 2010

Obesity and insulin resistance are very frequently associated to the metabolic syndrome (MetS), play a pivotal role in the development of type 2 diabetes mellitus (T2DM) and increases the risk of cardiovascular disease. Although it varies among ethnic groups, the worldwide prevalence of MetS is 23% in young adults and increases with age. Remarkably, the prevalence of MetS is expected to rise during the next decades due to the acquisition of unhealthy life-style habits (sedentarism, smoking, unhealthy diet). A major pathological alteration present in the MetS is a prothrombotic state resulting from endothelial dysfunction and hypercoagulability produced by a dysbalance of coagulation factors and proteins regulating fibrinolysis. Although intensive research in recent years has identified a number of prothrombotic alterations in MetS patients, a better understanding of the molecular mechanisms underlying the relationship between MetS and atherotrombosis is required to improve prevention and treatment. In this review we discuss the main alterations in the endothelial function, coagulation cascade, fibrinolysis and platelet function promoting atherothrombosis in MetS and available mouse models exhibiting alterations in atherothrombosis.

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