Inflammation is recognized as a fundamental element in the development and
growth of aortic aneurysms. Aortic aneurysm is correlated with aortic wall deformities and
injury, as a result of inflammation, matrix metalloproteinases activation, oxidative stress, and
apoptosis of vascular smooth muscle cells. The endothelial wall has a critical part in the inflammation
of the aorta and endothelial heterogeneity has proven to be significant for modeling
aneurysm formation. Endothelial shear stress and blood flow affect the aortic wall through
hindrance of cytokines and adhesion molecules excreted by endothelial cells, causing reduction
of the inflammation process in the media and adventitia. This pathophysiological process
results in the disruption of elastic fibers, degradation of collagen fibers, and destruction of
vascular smooth muscle cells. Consequently, the aortic wall is impaired due to reduced thickness,
decreased mechanical function, and cannot tolerate the impact of blood flow leading to
aortic expansion. Surgery is still considered the mainstay therapy for large aortic aneurysms.
The prevention of aortic dilation, though, is based on the hinderance of endothelial dysregulation
with drugs, the reduction of reactive oxygen and nitrogen species, and also the reduction
of pro-inflammatory molecules and metalloproteinases. Further investigations are required to
enlighten the emerging role of endothelial cells in aortic disease.