Rabia, Bibi, Thanigaimani, Shivshankar, and Golledge, Jonathan (2024) The potential involvement of glycocalyx disruption in abdominal aortic aneurysm pathogenesis. Cardiovascular Pathology, 70. 107629.

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Abstract

Background: 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.

Objective: The aim of this review was to identify a potential relationship between glycocalyx disruption and abdominal aortic aneurysm pathogenesis.

Methods: A narrative review of relevant published research was conducted.

Results: 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.

Conclusion: 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.

Item ID:	85860
Item Type:	Article (Research - C1)
ISSN:	1879-1336
Copyright Information:	© 2024 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)
Date Deposited:	17 Jun 2025 03:09
FoR Codes:	32 BIOMEDICAL AND CLINICAL SCIENCES > 3201 Cardiovascular medicine and haematology > 320101 Cardiology (incl. cardiovascular diseases) @ 100%
SEO Codes:	20 HEALTH > 2001 Clinical health > 200105 Treatment of human diseases and conditions @ 100%
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