Can Endothelial Glycocalyx Be a Major Morphological Substrate in Pre-Eclampsia?

Today pre-eclampsia (PE) is considered as a disease of various theories; still all of them agree that endothelial dysfunction is the leading pathogenic factor. Endothelial dysfunction is a sequence of permanent immune activation, resulting in the change of both the phenotype and the functions of an...

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Bibliographic Details
Published in:International journal of molecular sciences 2020-04, Vol.21 (9), p.3048
Main Authors: Ziganshina, Marina M, Yarotskaya, Ekaterina L, Bovin, Nicolai V, Pavlovich, Stanislav V, Sukhikh, Gennady T
Format: Article
Language:English
Subjects:
Activation
Carbohydrates
Cell adhesion & migration
Cell membranes
Chromatography
Congenital diseases
Drug development
Edema
Endothelial cells
endothelial glycocalyx
Endothelium
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Female
Gene Expression Regulation
Glycocalyx - metabolism
Glycocalyx - pathology
Heparan sulfate
Humans
Hypertension
Immune response
Immunosuppressive agents
Ischemia
Kidney diseases
Morphology
Mortality
Pathogenesis
Permeability
Phenotypes
Pre-eclampsia
Pre-Eclampsia - metabolism
Pre-Eclampsia - pathology
Preeclampsia
Pregnancy
Rehabilitation
Review
systemic inflammatory response
Veins & arteries
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Summary:Today pre-eclampsia (PE) is considered as a disease of various theories; still all of them agree that endothelial dysfunction is the leading pathogenic factor. Endothelial dysfunction is a sequence of permanent immune activation, resulting in the change of both the phenotype and the functions of an endothelial cell and of the extracellular layer associated with the cell membrane-endothelial glycocalyx (eGC). Numerous studies demonstrate that eGC mediates and regulates the key functions of endothelial cells including regulation of vascular tone and thromboresistance; and these functions are disrupted during PE. Taking into account that eGC and its components undergo alterations under pathological conditions leading to endothelial activation, it is supposed that eGC plays a certain role in pathogenesis of PE. Envisaging the eGC damage as a key factor of PE, might be a new approach to prevention, treatment, and rehabilitation of patients with PE. This approach could include the development of drugs protecting eGC and promoting regeneration of this structure. Since the issue of PE is far from being solved, any effort in this direction might be valuable.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21093048