Title:The Role of Endothelial Dysfunction in Aortic Aneurysms
Volume: 21
Issue: 28
Author(s): Gerasimos Siasos, Konstantinos Mourouzis, Evangelos Oikonomou, Sotirios Tsalamandris, Vasiliki Tsigkou, Konstantinos Vlasis, Manolis Vavuranakis, Thodoris Zografos, Stathis Dimitropoulos, Theodore G. Papaioannou, Aimilios Kalampogias, Christodoulos Stefanadis, Athanasios G. Papavassiliou and Dimitris Tousoulis
Affiliation:
Keywords:
Aortic aneurysms, atherosclerosis, cardiovascular diseases, endothelial dysfunction, endothelium vascular, inflammation.
Abstract: Abdominal aortic aneurysm is a vascular disease which, despite the fact that it shares common risk factors
with atherosclerosis, develops in parallel but as a partly independent process, through different pathogenic
mechanisms. The pathogenic mechanisms involve metalloproteinase and collagenase activation, median and adventitial
degradation, elastin lysis, vascular smooth cells transformation and apoptosis, collagen production and lysis
imbalance combined with excessive inflammatory infiltration. Endothelial cells respond to a number of stimulating
factors, including smoking, hypertension and AT1 receptor stimulation and non-uniform distribution of wall
stress. Their ability to produce NO is crucial in order to adapt. Endothelial cells contribute to AAA development
due to increased oxidative stress which is partly mediated by impaired NO bioavailability due to endothelial dysfunction
and NADPH oxidase overexpression. In addition, they express several molecules among which adherence
molecules, selectins, endothelin-1, regulating inflammatory infiltration and oxidative stress. Inflammatory cells consist of monocytes, polymorphonuclear
neutrophils and lymphocytes and they are involved in the degrading process in the aortic wall by secreting proteolytic
enzymesor by releasing interleukins which mediate the inflammation response. Endothelial dysfunction and arterial stiffness reflect on
indices like FMD, carotid-femoral PWV and augmentation index, sometimes with controversial results. At present, surgical treatment is
the only option provided in patients with large AAA, in particular. Focusing on the emerging role of endothelial cells in AAA pathology
may contribute in creating new therapeutic options in a disease which has not yet a well-accepted, implemented pharmaceutical treatment.
