Endothelial glycocalyx damage underlies the generalized endothelial dysfunction in preeclampsia

Area of Science:

• Obstetrics and Gynecology
• Vascular Biology
• Immunology

Background:

• Preeclampsia pathogenesis involves endothelial dysfunction, maternal-fetal immune maladaptation, and antiangiogenic factors.
• Previous research elucidated these factors in isolation, but their integrated role in preeclampsia remains unclear.
• Endothelial glycocalyx perturbation is implicated but not fully understood as a unifying mechanism.

Purpose of the Study:

• To comprehensively review the role of endothelial glycocalyx disruption in preeclampsia.
• To establish glycocalyx injury as a common link connecting diverse preeclamptic alterations across maternal organs.

Main Methods:

• Literature review synthesizing findings from human studies and animal models.
• Analysis of the pathophysiological consequences of glycocalyx perturbation on endothelial function.
• Integration of immunological and vascular aspects of preeclampsia.

Main Results:

• Endothelial glycocalyx perturbation leads to increased permeability and exposure of cell membranes.
• Loss of glycocalyx function impairs regulation of platelet aggregation, thrombosis, and leukocyte migration.
• Leukocyte migration and inflammation disrupt placental, renal, hepatic, cardiac, pulmonary, and cerebral function, manifesting as preeclampsia.

Conclusions:

• Endothelial glycocalyx disruption is a pivotal mechanism in preeclampsia.
• Glycocalyx injury unifies the understanding of maternal organ involvement in preeclampsia.
• Targeting glycocalyx integrity may offer novel therapeutic strategies for preeclampsia.