The potential involvement of glycocalyx disruption in abdominal aortic aneurysm pathogenesis

• Published in: Cardiovascular pathology 2024-05, Vol.70, p.107629, Article 107629
• Main Authors: Rabia, Bibi, Thanigaimani, Shivshankar, Golledge, Jonathan
• Format: Article
• Language: English
• Subjects: Abdominal aortic aneurysm; Glycocalyx disruption; Vascular inflammation
• ISSN: 1054-8807; 1879-1336; 1879-1336
• DOI: 10.1016/j.carpath.2024.107629

•Glycocalyx (GC) disruption has been reported in human and rodent model abdominal aortic aneurysm (AAA) samples.•GC disruption promotes vascular inflammation, matrix remodeling, and endothelial dysfunction implicated in AAA pathogenesis.•Deficiency of some of the GC components has been reported to promote AAA formation in rodent models. Abdominal aortic aneurysm is a weakening and expansion of the abdominal aorta. Currently, there is no drug treatment to limit abdominal aortic aneurysm growth. The glycocalyx is the outermost layer of the cell surface, mainly composed of glycosaminoglycans and proteoglycans. The aim of this review was to identify a potential relationship between glycocalyx disruption and abdominal aortic aneurysm pathogenesis. A narrative review of relevant published research was conducted. Glycocalyx 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 abdominal aortic aneurysm pathogenesis. Glycocalyx disruption promotes inflammation through exposure of adhesion molecules and release of proinflammatory mediators. Glycocalyx 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 abdominal aortic aneurysm pathogenesis. Deficiency of key component of the glycocalyx, such as syndecan-4, were reported to promote aneurysm formation and rupture in the angiotensin-II and calcium chloride induced mouse models of abdominal aortic aneurysm. This review provides a summary of past research which suggests that glycocalyx disruption may play a role in abdominal aortic aneurysm pathogenesis. Further research is needed to establish a causal link between glycocalyx disruption and abdominal aortic aneurysm development. The potential involvement of glycocalyx disruption in abdominal aortic aneurysm pathogenesis. AAA, abdominal aortic aneurysm; AT, antithrombin; CD44, cluster of differentiation 44; CS, chondroitin sulfate; ECM, extracellular matrix; eNOS, endothelial nitric oxide synthase; GC, glycocalyx; HA, hyaluronic acid; HS, heparan sulfate; ILT, intraluminal thrombus; MMPs, ma