Abstract
Background and Aims : Fibrillin-1 mutations result in rupture of the aorta, the main cause of mortality in patients with Marfan syndrome (MFS). When MTX is associated to LDE, the cell uptake is increased, which endows MTX with enhanced action mechanisms and the drug toxicity is diminished. The aims of this study was to investigate whether treatment with LDE-MTX can prevent the development of aortic arch lesions in a murine model of MFS.
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