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Pathophysiology of the proatherothrombotic state in the metabolic syndrome

AutorPalomo, Ivan; Moore-Carrasco, Rodrigo; Alarcón, Marcelo; Rojas, Armando; Espana, Francisco; Andrés, Vicente; González-Navarro, Herminia
Palabras clavemetabolic syndrome
endothelial dysfunction
plaque vulnerability
platelet activation
genetically-modified mice
Fecha de publicación1-ene-2010
EditorFrontiers in Bioscience Publications
CitaciónFrontiers in bioscience (Scholar edition) 2(1):194-208 (2010)
ResumenThe metabolic syndrome (MetS) is defined by the presence of at least three of the following abnormalities: glucose intolerance, hypertension, abdominal obesity, low HDL-cholesterol levels and hypertriglyceridemia. Obesity and insulin resistance are very frequently associated to the MetS and play a pivotal role in the development of type 2 diabetes mellitus (T2DM), which in turn 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 increase during the next decades due in part to the acquisition of unhealthy life-style habits (e.g., sedentarism, smoking, unhealthy diet, etc). A major pathological alteration present in the MetS is a prothrombotic state as a result of endothelial dysfunction and hypercoagulability produced by a dysbalance of coagulation factors and proteins involved in the regulation of fibrinolysis. Although intensive research in recent years has permitted the identification of 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 preventive and therapeutic strategies. In this review we discuss the main alterations in the endothelial function, coagulation cascade, fibrinolysis and platelet function that promote atherothrombosis in MetS patients. We also review available mouse models exhibiting alterations in atherothrombosis.
Descripción15 pages, 1 figure.--PMID: 20036940 [PubMed]
Versión del editorhttp://dx.doi.org/10.2741/57
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