The Potential Involvement of Glycocalyx Disruption in Abdominal Aortic Aneurysm Pathogenesis

Background Abdominal aortic aneurysm (AAA) is a weakening and expansion of the abdominal aorta. Currently, there is no drug treatment to limit AAA growth. The glycocalyx (GC) is the outermost layer of the cell surface, mainly composed of glycosaminoglycans (GAGs) and proteoglycans. Objective The aim of this review was to identify a potential relationship between GC disruption and AAA pathogenesis. Methods A narrative review of relevant published research was conducted. Results GC disruption has been reported to enhance vascular permeability, impair immune responses, dysregulate endothelial function, promote extracellular matrix remodeling and modulate mechanotransduction. All these effects are implicated in AAA pathogenesis. GC disruption promotes inflammation through exposure of adhesion molecules and release of proinflammatory mediators. GC disruption affects how the endothelium responds to shear stress by reducing nitric oxide availabilty and adversely affecting the storage and release of several antioxidants, growth factors and antithromotic proteins. These changes exacerbate oxidative stress, stimulate vascular smooth muscle cell dysfunction and promote thrombosis, all effects implicated in AAA pathogenesis. Deficiency of key component of the GC, such as syndecan-4, were reported to promote aneurysm formation and rupture in the angiotensin-II and calcium chloride induced mouse models of AAA. Conclusion This review provides a summary of past research which suggests that GC disruption may play a role in AAA pathogenesis. Further research is needed to establish a causal link between GC disruption and AAA development.