Endothelium in Aortic Aneurysm Disease: New Insights

Abstract

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.