Review of the Techniques Used for Investigating the Role Elastin and Collagen Play in Arterial Wall Mechanics

Abstract

The arterial wall is characterised by a complex microstructure that impacts the mechanical properties of the vascular tissue. The main components consist of collagen and elastin fibres, proteoglycans, Vascular Smooth Muscle Cells (VSMCs) and ground matrix. While VSMCs play a key role in the active mechanical response of arteries, collagen and elastin determine the passive mechanics. Several experimental methods have been designed to investigate the role of these structural proteins in determining the passive mechanics of the arterial wall. Microscopy imaging of load-free or fixed samples provides useful information on the structure-function coupling of the vascular tissue, and mechanical testing provides information on the mechanical role of collagen and elastin networks. However, when these techniques are used separately, they fail to provide a full picture of the arterial micromechanics. More recently, advances in imaging techniques have allowed combining both methods, thus dynamically imaging the sample while loaded in a pseudo-physiological way, and overcoming the limitation of using either of the two methods separately. The present review aims at describing the techniques currently available to researchers for the investigation of the arterial wall micromechanics. This review also aims to elucidate the current understanding of arterial mechanics and identify some research gaps.

From Uniaxial Testing of Isolated Layers to a Tri-Layered Arterial Wall: A Novel Constitutive Modelling Framework

“…Elastin and collagen are commonly considered the major determinants of the passive mechanical response of arteries, as smooth muscle cells have a relatively low passive stiffness. 5,14,45 As reported in several studies, the relative amount, as well as the spatial organisation, of elastin and collagen fibres varies considerably across the arterial wall, 14,22,25 conferring different mechanical properties and function to the intimal, medial, and adventitial layers. The intima directly interfaces with the blood flow and has a marginal contribution the overall wall mechanics of young healthy arteries.…”

“…(11), while wall stresses were calculated from the layers' stresses using Eq. (14). The circumferential material stiffness was calculated according to two different formulations: first, K hhhh was calculated as the tangent elastic modulus in the circumferential stress-circumferential strain relationship, 24 and, sec-ond, C hhhh was calculated according to the small-onlarge formulation 1 :…”

Subject-Specific Pressure Normalization of Local Pulse Wave Velocity: Separating Intrinsic From Acute Load-Dependent Stiffening in Hypertensive Patients

“…Arterial stiffness as pulse wave velocity (PWV) is a powerful predictor of mortality and cardiovascular events in hypertensive patients, above and beyond traditional risk factors (Boutouyrie et al, 2002;Laurent et al, 2003;Cardoso et al, 2019). The arterial wall, however, presents a complex microstructure where different wall constituents, mainly collagen, elastin, and smooth muscle, play different but equally important roles in arterial function (Boutouyrie et al, 1998;Cruickshank et al, 2002;Krasny et al, 2017;Giudici et al, 2021e). The heterogeneous microstructure of the arterial wall makes its behavior highly nonlinear (Giudici et al, 2021b) so that arterial stiffness and, consequently, PWV are intrinsically blood pressure (BP)-dependent (Spronck et al, 2015b).…”

Comparative therapeutic strategies for preventing aortic rupture in a mouse model of vascular Ehlers-Danlos syndrome

“…The main role of collagen in arteries is the maintenance of arterial structure and resistance to arterial blood pressure. Indeed collagen fibers are stretched at higher than normal pressures and have a protective supporting role, whereas elastic fibers characterized by their great range of extensibility limit the normal blood pressure (BP) fluctuations [ 7 ]. In vEDS patients, the marked arterial fragility caused by the deficit in collagen III is associated with thinner arterial wall and slightly increased stiffness at diastolic blood pressure [ 8 , 9 ].…”