Abdominal aortic aneurysm (AAA) is a multifactorial and heterogeneous cardiovascular disorder, manifested as a local dilatation of the infrarenal aorta of 3.0 cm or more, which predisposes the abdominal aorta to rupture. Data from population studies have shown a predisposition to aneurysm in 4 to 7 % of men and in 1 to 2 % of women aged 65 [1,2]. The asymptomatic nature of the condition often results in delayed diagnosis, with symptoms manifesting only in the advanced stages of the disease, which contributes to the associated high mortality rate. AAA is responsible for approximately 170,000 deaths worldwide each year [3]. Study reports suggest that no single factor can be blamed for a predisposition to AAA. It is a complex disorder involving both environmental and genetic factors that disrupt the normal structure of the aorta and lead to the development of AAA [4]. The primary risk factors associated with the development of an aneurysm include smoking, male gender, and having a relative with an aneurysm [[5], [6], [7]].

The aorta is the largest elastic artery, consisting of three layers: tunica intima, tunica media, and tunica adventitia. Each layer contains components that help maintain vessel homeostasis. The tunica intima is lined with endothelial cells and contains collagen types III and IV, which regulate inflammation and vessel contraction [[8], [9], [10], [11]]. The tunica media is composed of smooth muscle cells and collagen I, providing strength, and elastin, enabling elastic stretching and contraction [8,9]. The tunica adventitia contains fibroblasts and collagen I, providing structural integrity and protection, with fewer elastin fibers than the middle layer [8,11].

AAA development is characterized by considerable variability. Based on our previous observations, we hypothesized that AAAs exhibit substantial heterogeneity along their length. To test this, we developed a method for dividing AAAs into defined segments and layers, which we applied in all experiments [[12], [13], [14], [15]]. In vitro, we observed that isolated cells gradually lost their characteristic markers [13,15]. We also assessed the expression of matrix metalloproteinases (MMPs), their inhibitors (TIMPs), and members of the disintegrin and metalloproteinase family with thrombospondin motifs (ADAMTS) [12]. Distinct expression patterns were observed along the aorta, with significant regional differences between proximal and distal segments. Furthermore, the expression of thrombospondin genes (THBS1, THBS2, THBS3) was markedly higher in AAA tissue compared to controls, particularly in the case of THBS3 [14]. Our studies have shown that cells involved in maintaining aortic wall homeostasis, together with MMPs and other key ECM molecules, influence the synthesis, degradation, and/or redistribution of elastin and collagen across the different layers of the vessel wall. However, to date, there is a lack of scientific reports that could provide a comprehensive overview of AAA variability at the histological and molecular levels in individual sections and layers. Therefore, we hypothesized that AAA is variable along its entire length. To prove our hypothesis, we evaluated histologically collagen I and III, elastin, and the presence of smooth muscle cells in AAA tissue. Moreover, we analyzed the expression of COL1A1, COL1A2, COL3A1, and ELN genes as well as the α-chains of collagen I and III and elastin at the protein level.