Limitations and risks associated with the current clinical assessment of aortic ruptures call for a better understanding of aortic biomechanics, and glycosaminoglycan (GAGs) and proteoglycans (PGs) have emerged as influencing components. GAGs are highly negatively charged polysaccharide molecules. These and PGs, which comprise a protein core with one or more covalently-bound GAGs molecule, are present in the extracellular matrix of the arterial wall. In this review, we discuss the potential mechanical roles of GAGs/PGs in the aorta, and highlight their fundamental swelling behavior as a potential contributor to residual stresses. GAGs/PGs are heterogeneously distributed in the aortic wall, and deciphering the relationship between their intramural distribution and that of swelling could help better understand residual stresses. Residual stresses, in turn, are fundamental to the accurate evaluation of mural mechanical stresses. This underlines the significance of taking GAGs/PGs into account in mathematical and numerical models, and calls for improved quantitative layer specific characterization of GAGs/PGs in the aortic wall. We also reveal gaps in the current understanding of GAGs/PGs with regards to aortic stiffness, specifically, as to whether the reduction of these polyanionic molecules causes an increase, or a decrease, in aortic stiffness. This review finally underscores GAGs/PGs as important components in aortic disease, namely in thoracic aortic aneurysm (TAAD) and abdominal aortic aneurysm (AAA). While overall GAGs/PGs accumulate in TAAD and diminish in AAA, questions remain regarding small PGs. Since GAGs/PGs pooling in TAAD could potentially lead to stress concentrations that surpass the rupture threshold, causing a delamination to initiate and propagate, there is a need to understand which levels of GAGs/PGs exist in physiological and pathological aortas. In AAA, there is still no clear indication whether or not any relationship exists between the marked reduction in GAG/PG content, and the ongoing stiffening and weakening of the aortic wall.
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