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Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2200-2207
Published online before print August 24, 2006, doi: 10.1161/01.ATV.0000242905.41404.68
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2200.)
© 2006 American Heart Association, Inc.


Brief Reviews

PAI-1 and the Metabolic Syndrome

Links, Causes, and Consequences

Marie-Christine Alessi; Irène Juhan-Vague

From the Laboratory of Hematology, INSERM UMR 626, Faculty of Medicine, Marseilles, France.

Correspondence to Irène Juhan-Vague, Laboratoire d’hématologie, Inserm UMR 626, Faculté de Médecine, 27, bd Jean Moulin, 13385 Marseille cedex 5, France. E-mail ijuhan{at}ap-hm.fr

The link between plasminogen activator inhibitor (PAI)-1 and the metabolic syndrome with obesity was established many years ago. Increased PAI-1 level can be now considered a true component of the syndrome. The metabolic syndrome is associated with an increased risk of developing cardiovascular disease, and PAI-1 overexpression may participate in this process. The mechanisms of PAI-1 overexpression during obesity are complex, and it is conceivable that several inducers are involved at the same time at several sites of synthesis. Interestingly, recent in vitro and in vivo studies showed that besides its role in atherothrombosis, PAI-1 is also implicated in adipose tissue development and in the control of insulin signaling in adipocytes. These findings suggest PAI-1 inhibitors serve in the control of atherothrombosis and insulin resistance.

The metabolic syndrome is associated with overexpression of PAI-1; the mechanisms involved are complex. Besides its role in atherothrombosis, PAI-1 is also implicated in obesity and insulin resistance. The development of PAI-1 inhibitors is a challenge.


Key Words: adipose tissue • atherothrombosis • metabolic syndrome • obesity • PAI-1




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