Endothelial glycocalyx as a potential theriapeutic target in organ injuries.
10.1097/CM9.0000000000000177
- Author:
Rui-Na CAO
1
;
Li TANG
1
;
Zhong-Yuan XIA
2
;
Rui XIA
1
Author Information
1. Department of Anesthesiology, The First Affiliated Hospital of Yangtze University, Jingzhou, Hubei 434000, China.
2. Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430061, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Databases, Factual;
Endothelium, Vascular;
metabolism;
pathology;
Glycocalyx;
metabolism;
pathology;
Humans;
Shear Strength
- From:
Chinese Medical Journal
2019;132(8):963-975
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:The endothelial glycocalyx (eGC) is a dynamic and multicomponent layer of macromolecules found at the surface of vascular endothelium, which is largely underappreciated. It has recently been recognized that eGC is a major regulator of endothelial function and may have therapeutic value in organ injuries. This study aimed to explore the role of the eGC in various pathologic and physiologic conditions, by reviewing the basic research findings pertaining to the detection of the eGC and its clinical significance. We also explored different pharmacologic agents used to protect and rebuild the eGC.
DATA SOURCES:An in-depth search was performed in the PubMed database, focusing on research published after 2003 with keywords including eGC, permeability, glycocalyx and injuries, and glycocalyx protection.
STUDY SELECTION:Several authoritative reviews and original studies were identified and reviewed to summarize the characteristics of the eGC under physiologic and pathologic conditions as well as the detection and protection of the eGC.
RESULTS:The eGC degradation is closely associated with pathophysiologic changes such as vascular permeability, edema formation, mechanotransduction, and clotting cascade, together with neutrophil and platelet adhesion in diverse injury and disease states including inflammation (sepsis and trauma), ischemia-reperfusion injury, shock, hypervolemia, hypertension, hyperglycemia, and high Na as well as diabetes and atherosclerosis. Therapeutic strategies for protecting and rebuilding the eGC should be explored through experimental test and clinical verifications.
CONCLUSIONS:Disturbance of the eGC usually occurs at early stages of various clinical pathophysiologies which can be partly prevented and reversed by protecting and restoring the eGC. The eGC seems to be a promising diagnostic biomarker and therapeutic target in clinical settings.
