Vascular repair by endothelial progenitor cells in an experimental model of metabolic syndrome

Abstract

Feeding carbohydrate-enriched diets to normal rats has been shown to induce metabolic syndrome. Fructose-fed rats (FFR) have been used to assess the pathophysiological mechanisms involved in the development of this syndrome. The best finding in this study are the description of vascular inflammation associated with mesenteric remodeling in experimental models that received fructose and the vascular repair found in association with a smaller expression of CD34/Flk-1+ cells in the vascular wall of mesenteric arteries, a greater number of CD34+ cells expressed in the vascular wall probably participates actively in the pathophysiology of vascular remodeling in this experimental model. This finding can partly contribute to elaborate new tools, nonpharmacological or pharmacological, to diminish the final organ damage undergone by this experimental model, thus lowering the cardiovascular risk of developing atherosclerotic disease and therefore myocardial infarction or stroke.