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. 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 affects 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 hinder of endothelial dysregulation with drugs, reduction of reactive
oxygen and nitrogen species, and reduction of pro-inflammatory molecules and
metalloproteinases. Further investigations are required to enlighten the emerging role of
endothelial cells in aortic disease.