## 1 Introduction  
The aorta is the primary artery through which blood leaves the human heart before it flows through the entire human body, and it is typically divided into several sections based on anatomical source, as shown in Figure 1[1; 2; 3; 4]. Based on the anatomical compartment, it is categorized as the thoracic aorta from the heart to the diaphragm and the abdominal aorta from the diaphragm to the bifurcation of the aorta, respectively. Another classification method classifies the aorta according to its route and blood flow direction. Hence, the aorta goes out from the heart and down as the ascending aorta and then performs a hairpin turn. Following this, the aorta runs as the descending aorta, which is divided into two major parts: thoracic aorta and abdominal aorta. The aorta ends at a bifurcation, which is divided into two main blood vessels: the common iliac arteries and a smaller midline vessel, the median sacral artery [5]. The aorta exhibits the characteristics of a hyper-elastic and viscoelastic material. It is composed of a heterogeneous mixture of smooth muscle nerves, endothelial cells, intimal cells, fibroblast-like cells, and a complex extracellular matrix. The arterial wall consists of three layers, intima, media, and adventitia. In particular, the smooth muscles and extracellular matrix are the largest components of the arterial wall in the media layer. Specifically, the media layer of the arterial wall consists of concentric elastic lamella, namely smooth muscles and an elastic matrix. The smooth muscle component does not transform the diameter of the aorta significantly; instead, it serves to increase the stiffness and viscoelasticity of the aortic wall when activated. The elastic matrix controls the biomechanical properties of the aorta and forms lamellae consisting of elastic fibers, collagens, proteoglycans, and glycosaminoglycans [6]. Thus, the vascular smooth muscle cells can make significant contributions to aortic stiffness, and many studies have been conducted on them. In particular, [PERSON] et al. [7,8] measured the mouse aortic mechanical properties in order to assess the vascular smooth muscle cell component of stiffness in the aortic wall according to age. In addition, they examined the mechanical properties of blood vessels across multiple length scales and identified the focal adhesion of the vascular smooth muscle cells. [PERSON] et al. [9] determined whether vascular smooth muscle cells adhesion to type I collagen was transformed in parallel with the changes in the vascular smooth muscle cells' contractile state induced by vasoconstristors and vasodilators, and they proposed that the signal transduction pathways modulating vascular smooth muscle cell contractile activation and relaxation, as well as extracellular matrix adhesion interact during regulation of the contractile state. [PERSON] et al. [10] investigated whether basal nitric oxide activity and voltage-gated Ca\({}^{2+}\) channel-mediated contractions differed between the smaller, muscular arteries (femoral and mesenteric arteries) and the larger, elastic conduit vessels (aorta and carotid artery) of mice. As a result, they assumed that the different physiological behavior of elastic and muscular arteries of young adults were linked to the well-known observation that arterial stiffness develops differently with aging. In addition to studies on vascular smooth muscle cells, studies on the properties of the aorta and diseases such as aortic aneurysm and aortic dissection have been conducted in the past few decades [11; 12; 13; 14; 15; 16; 17; 18; 19]. In particular, [PERSON] et al. [15] conducted biomechanical experiments on the porcine abdominal artery by uniaxial elongation and relaxation tests in both the circumferential and longitudinal directions and applied a combined logarithm and polynomial strain energy equation to model the elastic response of the specimens.