Aortic aneurysms are high-risk conditions that can lead to fatal outcomes. Current clinical evaluations primarily rely on measuring the aneurysm’s maximum diameter to estimate rupture risk. However, this criterion alone is often insufficient, as life-threatening events have occurred even below the threshold for surgical intervention. This highlights the importance of a deeper knowledge of disease progression to understand the complex pathophysiological mechanisms involved, such as the balance between wall stress and tissue resistance. In this study, we present a computational model for simulating the mechanobiological remodeling of arterial tissue, implemented in Abaqus through a custom UMAT subroutine. The vessel wall is modelled as an anisotropic hyperelastic material using the Holzapfel-Gasser-Ogden (HGO) formulation, which incorporates the effect of fiber orientation . To model the remodeling, a multiplicative decomposition of the deformation gradient F into a remodeling component and an elastic component was performed to ensure body’s continuity. Tissue remodeling is triggered by localized stiffening of the material properties, as seen in pathological arteries, and occurs only in regions with altered material properties through a one-way coupling. In this preliminary stage, the vessel is idealized as a simplified cylindrical geometry. The aneurysmal region is modelled with increased localized stiffening, triggering the remodelling process and representing pathological disease progression. Preliminary simulations show that the central pathological region undergoes remodeling accompanied by a marked reduction in tissue’s elastic properties. These results demonstrate the model's ability to reproduce key features of aneurysm evolution, both structurally and mechanobiologically. Future developments will focus on applying the model to patient-specific geometries to support more accurate and personalized risk assessments, ultimately contributing to improved clinical decision-making and treatment planning.