The Potential Involvement of Glycocalyx Disruption in Abdominal Aortic Aneurysm Pathogenesis.

Abdominal aortic aneurysm glycocalyx disruption vascular inflammation

Journal

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
ISSN: 1879-1336
Titre abrégé: Cardiovasc Pathol
Pays: United States
ID NLM: 9212060

Informations de publication

Date de publication:
08 Mar 2024
Historique:
received: 07 01 2024
revised: 03 03 2024
accepted: 04 03 2024
medline: 11 3 2024
pubmed: 11 3 2024
entrez: 10 3 2024
Statut: aheadofprint

Résumé

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. The aim of this review was to identify a potential relationship between GC disruption and AAA pathogenesis. A narrative review of relevant published research was conducted. 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. 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.

Sections du résumé

BACKGROUND 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 OBJECTIVE
The aim of this review was to identify a potential relationship between GC disruption and AAA pathogenesis.
METHODS METHODS
A narrative review of relevant published research was conducted.
RESULTS 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 CONCLUSIONS
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.

Identifiants

DOI: 10.1016/j.carpath.2024.107629 PMID: 38461960
pubmed: 38461960
pii: S1054-8807(24)00025-5
doi: 10.1016/j.carpath.2024.107629
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

107629

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Bibi Rabia (B)

Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, Queensland 4811, Australia; Department of Pharmacy, Hazara University, Mansehra 21300, Pakistan.

Shivshankar Thanigaimani (S)

Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, Queensland 4811, Australia; The Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Queensland 4811, Australia.

Jonathan Golledge (J)

Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, Queensland 4811, Australia; The Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Queensland 4811, Australia; The Department of Vascular and Endovascular Surgery, The Townsville University Hospital, Townsville, Queensland 4810, Australia. Electronic address: jonathan.golledge@jcu.edu.au.

Classifications MeSH