## 1 Introduction  
The vascular system transports oxygen, nutrients, and waste products throughout the body to facilitate their exchange between different compartments [1]. Several diseases are associated with the cardiovascular system and affect both blood vessels and the heart. AAA is a stealthy ailment carrying an 85% fatality risk upon rupture, characterized by a weakening of the abdominal aorta's vessel walls, leading to their enlargement or dilation [2, 3]. AAA involves the calcification and infiltration of inflammatory cells and the degradation of elastic lamellae, remaining asymptomatic until a potentially catastrophic rupture event [4, 5]. Vascular calcification is one of the prevalent pathological conditions that affect human health in a severe manner [6]. Aortic calcification is associated with an increased risk of ruptured intracranial aneurysms [7]. Different factors increase the risk of developing vascular calcification, including aging, cardiovascular diseases, diabetes, chronic kidney diseases, etc. [8, 9, 10, 11]. Blood vessels, in particular arteries, are composed of three layers: tunica adventitia, which is the outermost connective tissue layer; tunica media, made up of smooth muscle cells and elastin in its extracellular matrix; and tunica intima, which consists of a single thin layer of endothelial cells [10]. Recent studies have identified vascular microcalcification as a novel pathological characteristic and a potential mediator of AAA, suggesting that targeting microcalcification may be a promising strategy for both prevention and treatment [12]. Vascular calcification is characterized by mineral deposition in the tunica media or intima. Intimal calcification mainly occurs in atherosclerosis, which is associated with inflammation, lipid deposition, and the formation of microcalcifications [10; 13]. Tunica media calcification is not entirely described; however, it is similar to intimal calcification as both processes resemble bone formation [14]. The primary outcome in tunica media calcification is vascular stiffness that leads to low vessel compliance, which can ultimately lead to an aortic aneurysm due to mechanical stress, highlighting the importance of understanding the underlying mechanisms of calcification in cardiovascular disease [15; 16]. Indeed, the exact molecular mechanism behind the development of vascular calcification has yet to be understood, possibly due to the involvement of several overlapping mechanisms. However, studies have shown that smooth muscle cells are involved in pathogenesis, differentiating into osteoblast-like cells and producing a calcifying matrix [17; 18; 19]. The exact signaling pathway is still under investigation. Different factors contribute to the initiation of this process. Such factors include the absence of calcification inhibitors, a rise in smooth muscle cell oxidants, damage to DNA, apoptosis, and disturbance of calcium-phosphate hemostasis [20]. In differentiated smooth muscle cells, bone-related transcription factors, which upregulate bone proteins, are detected [20]. Bone morphogenetic proteins and inflammation mediators like TNF\(\alpha\) are observed to activate the Mxs2 transcription factor that, in turn, activates other factors like Runx2 and osterix. Moreover, bone-related proteins, including osteoclast, sclerostin, RANKL, sialoprotein and alkaline phosphatase, are expressed and thus promote vascular calcification [20]. The induction of abdominal aortic injury through the administration of calcium chloride (CaCl\({}_{2}\)) has become a pivotal approach in vascular research, contributing significantly to our understanding of arterial pathology [21; 22]. This experimental model involves the topical application of CaCl\({}_{2}\) to the abdominal aorta, leading to localized injury and subsequent pathological changes. The injury induces a cascade of events, including inflammation, elastin degradation, and medial layer thinning, mimicking aspects of aortic aneurysm development [21; 23].