Marfan syndrome (MFS) (OMIM # 154700) is an autosomal dominant disease that has a mutation in the FBN1 gene, which encodes the fibrillin-1 protein, located in the aorta, heart, lung and kidney, Organs main organs in the cardiovascular axis. The fibrillin-1 defect plays a role in tissue remodeling, activating other ECM proteins, and Losartan® therapy has the potential to mitigate matrix changes in Marfan syndrome. Given the methodological limits in the clinic, it is usual to use experimental models to understand the intrinsic mechanisms of diseases. The mg∆ lpn model recapitulates the clinical changes and has a high survival rate. For this reason, the study aimed to analyze the structural repercussions of the cardiovascular axis organs in the mgΔlpn model and the influence of Losartan® therapy at 3 months and 6 months. In the present study, 72 mice were used, distributed in the groups: Savages (WT), mgΔ lpn (MFS), and mgΔlpn treated with Losartan® (MFSTrat). In each group, there were animals at the ages of 3 months and 6 months, with 12 animals per age. To characterize the changes in the model, the following techniques were used: x-ray, rtPCR, hemodynamic analysis, histomorphometry, ultrastructural, and immunohistochemistry (fibrillin-1; MMP-9; fibronectin and smooth muscle α-actin). The mg∆lpn model presented a defect in the thoracic spine, which had the ability to change the path of the aorta, changing the dynamics of blood flow. Once altered, the blood flow in the aorta overloads the heart, mainly hypertrophying the left ventricle. Concomitantly, the lung presented emphysema and the kidney showed a significant reduction in the glomerulus, vascular pole, and urinary space. In addition, there was a significant reduction in fibrillin-1 protein and an increase in MMP-9, both at 3 months and 6 months, indicating a progressive degradation of elastic fibers in all analyzed organs. Losartan® therapy showed effectiveness in phenotypic attenuation only at 3 months, increasing the expression of fibronectin and reducing the expression of MMP-9. Although changes in fibrillin-1 and MMP-9 proteins have been noted systemically, it was noted that tissue remodeling was organ dependent, in addition to having different responses over time, characteristics which will spur further future studies.