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Mechanisms of fibrinogen-induced microvascular dysfunction during cardiovascular disease

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Fibrinogen (Fg) is a high molecular weight plasma adhesion protein and a biomarker of inflammation. Many cardiovascular and cerebrovascular disorders are accompanied by increased blood content of Fg. Increased levels of Fg result in changes in blood rheological properties such as increases in plasma viscosity, erythrocyte aggregation, platelet thrombogenesis, alterations in vascular reactivity and compromises in endothelial layer integrity. These alterations exacerbate the complications in peripheral blood circulation during cardiovascular diseases such as hypertension, diabetes and stroke. In addition to affecting blood viscosity by altering plasma viscosity and erythrocyte aggregation, growing experimental evidence suggests that Fg alters vascular reactivity and impairs endothelial cell layer integrity by binding to its endothelial cell membrane receptors and activating signalling mechanisms. The purpose of this review is to discuss experimental data, which demonstrate the effects of Fg causing vascular dysfunction and to offer possible mechanisms for these effects, which could exacerbate microcirculatory complications during cardiovascular diseases accompanied by increased Fg content.

Keywords: Weibel-Palade body exocytosis; arteriolar constriction; endothelial cell layer permeability; endothelin-1; erythrocyte aggregation; tight junction proteins

Document Type: Research Article


Affiliations: 1:  Department of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY, USA 2:  Department of Biochemistry and Molecular Biology, School of Medicine, University of Louisville, Louisville, KY, USA

Publication date: January 1, 2010


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