Endothelial glycocalyx damage underlies the generalized endothelial dysfunction in preeclampsia.

In pregnancy, endothelial dysfunction serves as a key mechanism linking maternal-fetal immune maladaptation and soluble antiangiogenic factors to the clinical presentation of preeclampsia. Although most of these aspects have been elucidated in isolation in humans and in animal models, a complete picture of their relationship with the clinical manifestations of preeclampsia has been elusive. Perturbation of endothelial glycocalyx results from conflicting inflammatory messages and leads to a paradoxical situation involving tissue distress and stimulation of maternal syndrome. Increased endothelial permeability and exposure of the endothelial cell membrane are key to the pathogenesis of this syndrome. Nude membranes, which flack the glycocalyx cover, lose critical functions in modulating local platelet aggregation, thrombosis, inflammation, and leukocyte migration. Leukocyte migration into tissues and subsequent inflammation alter the normal functioning of important organs such as the placenta, maternal kidney, liver, heart, lung, and brain, and consequently lead to the broad spectrum of clinical manifestations of preeclampsia. Moreover, glycocalyx injury has an important role underlying the mechanisms leading to diverse forms of preeclampsia. Herein, we provide a comprehensive view of glycocalyx disruption as the common link among the preeclamptic alterations observed in all maternal organs.