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PAI-1, Obesity, and Insulin Resistance

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Insulin Resistance

Abstract

Thrombosis favors the development of vascular damage and is responsible for many complications of atherosclerosis. It occurs primarily at the site of a ruptured atherosclerotic plaque and can be incorporated into the vascular wall. This event is partly determined by the thrombotic/thrombolytic equilibrium at the time of plaque rupture. Thrombolytic potential is mainly under the control of an inhibitor of plasminogen activation (PAI-1), whose modulation has been shown to influence fibrin and extracellular matrix accumulation. Elevated PAI-1 concentration in plasma is presently considered a risk factor for coronary vascular events (1,2). Moreover, an elevation of circulating PAI-1 has been shown to be associated with insulin-resistance with obesity and noninsulin dependent diabetes (3). It has thus been postulated (3) that PAI-1 could contribute to increased susceptibility to atherothrombosis in insulin-resistant patients (4–9). The elucidation of the regulation of PAI-1 synthesis and the identification of factors responsible for increased plasma PAI-1 concentration in the insulin resistance states might lead to therapeutic concepts for prevention of vascular lesions.

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Juhan-Vague, I., Alessi, MC., Morange, P.E. (1999). PAI-1, Obesity, and Insulin Resistance. In: Reaven, G.M., Laws, A. (eds) Insulin Resistance. Contemporary Endocrinology, vol 12. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-716-1_17

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