Molecular and Cellular Mechanisms Involved in Aortic Wall Aneurysm Development

Abstract

Aortic aneurysms represent a very common pathology that can affect any segment of the aorta. These types of aneurysms can be localized on the thoracic segment or on the abdominal portion, with the latter being more frequent. Though there are similarities between thoracic and abdominal aortic aneurysms, these pathologies are distinct entities. In this article, we undertook a review regarding the different mechanisms that can lead to the development of aortic aneurysm, and we tried to identify the different manners of treatment. For a long time, aortic wall aneurysms may evolve in an asymptomatic manner, but this progressive dilatation of the aneurysm can lead to a potentially fatal complication consisting in aortic rupture. Because there are limited therapies that may delay or prevent the development of acute aortic syndromes, surgical management remains the most common manner of treatment. Even though, surgical management has improved much in the last years, thus becoming less invasive and sophisticated, the morbi-mortality linked to these therapies remains increased. The identification of the cellular and molecular networks triggering the formation of aneurysm would permit the discovery of modern therapeutic targets. Molecular and cellular mechanisms are gaining a bigger importance in the complex pathogenesis of aortic aneurysms. Future studies must be developed to compare the findings seen in human tissue and animal models of aortic aneurysm, so that clinically relevant conclusions about the aortic aneurysm formation and the pharmacological possibility of pathogenic pathways blockage can be drawn.

N6-methyladenosine-associated genetic variants in NECTIN2 and HPCAL1 are risk factors for abdominal aortic aneurysm

“…Our enrichment analysis revealed that the DEGs in which m6A-SNPs located could participate in T cell receptor signaling pathway, immune response, cell adhesion, vascular smooth muscle contraction, calcium signaling pathway, gap junction, Wnt signaling pathway et al. These predictive features are closely related to the regulation of AAA development, 27 , 28 indicating a connection between m6A-SNPs and biological processes or signaling pathways associated with AAA pathogenesis.…”

ER stress mediates Angiotensin II-augmented innate immunity memory and facilitates distinct susceptibilities of thoracic from abdominal aorta to aneurysm development

“…The aortic arch and thoracic aorta develop higher incidences of atherosclerosis but a relatively lower incidence of Ang II-induced aortic aneurysm ( 33 – 37 ) than the abdominal aorta in the HFD-fed ApoE-KO plus Ang II infusion model ( Figure 1A ). However, the detailed transcriptomic mechanisms underlying the phenotypic differences remained poorly defined ( 5 , 38 – 40 ). To determine the transcriptomic mechanisms, we performed RNA-Seq analysis to determine transcriptomic differences between the abdominal aorta and the thoracic aorta in AAA.…”

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

“…MMP-12 can degrade elastin and plays a key role in macrophage migration. MMP-12 expression is increased in the case of AAA [127].…”