Therapeutic strategies targeting the endothelial glycocalyx.


Journal

Current opinion in clinical nutrition and metabolic care
ISSN: 1473-6519
Titre abrégé: Curr Opin Clin Nutr Metab Care
Pays: England
ID NLM: 9804399

Informations de publication

Date de publication:
01 11 2023
Historique:
pmc-release: 01 11 2024
medline: 10 10 2023
pubmed: 9 8 2023
entrez: 9 8 2023
Statut: ppublish

Résumé

This review will highlight recent studies that have examined the endothelial glycocalyx in a variety of health conditions, as well as potential glycocalyx-targeted therapies. A degraded glycocalyx is present in individuals that consume high sodium diet or have kidney disease, diabetes, preeclampsia, coronavirus disease 2019 (COVID-19), or sepsis. Specifically, these conditions are accompanied by elevated glycocalyx components in the blood, such as syndecan-1, syndecans-4, heparin sulfate, and enhanced heparinase activity. Impaired glycocalyx barrier function is accompanied by decreased nitric oxide bioavailability, increased leukocyte adhesion to endothelial cells, and vascular permeability. Glycocalyx degradation appears to play a key role in the progression of cardiovascular complications. However, studies that have used glycocalyx-targeted therapies to treat these conditions are scarce. Various therapeutics can restore the glycocalyx in kidney disease, diabetes, COVID-19, and sepsis. Exposing endothelial cells to glycocalyx components, such as heparin sulfate and hyaluronan protects the glycocalyx. We conclude that the glycocalyx is degraded in a variety of health conditions, although it remains to be determined whether glycocalyx degradation plays a causal role in disease progression and severity, and whether glycocalyx-targeted therapies improve patient health outcomes. Future studies are warranted to investigate therapeutic strategies that target the endothelial glycocalyx.

Identifiants

pubmed: 37555800
doi: 10.1097/MCO.0000000000000973
pii: 00075197-990000000-00103
pmc: PMC10592259
mid: NIHMS1921135
doi:

Substances chimiques

Heparin 9005-49-6
Sulfates 0

Types de publication

Review Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

543-550

Subventions

Organisme : NCCIH NIH HHS
ID : R00 AT010017
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG050238
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG060395
Pays : United States
Organisme : NIA NIH HHS
ID : R44 AG053131
Pays : United States

Informations de copyright

Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.

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Auteurs

Daniel R Machin (DR)

Department of Nutrition and Integrative Physiology, Florida State University, Tallahassee, Florida.

Mostafa Sabouri (M)

Department of Nutrition and Integrative Physiology, Florida State University, Tallahassee, Florida.

Xiangyu Zheng (X)

Department of Nutrition and Integrative Physiology, Florida State University, Tallahassee, Florida.

Anthony J Donato (AJ)

Department of Internal Medicine, University of Utah, Utah.
Geriatric Research, Education, and Clinical Center, Salt Lake City Veterans Affairs Medical Center, VA SLC.
Department of Nutrition and Integrative Physiology.
Department of Biochemistry.
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah, USA.

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Classifications MeSH