Placenta and maternal endothelium during preeclampsia: Disruption of the glycocalyx explains increased inositol phosphoglycans and angiogenic factors in maternal blood

Scioscia, Marco; Siwetz, Monika; Robillard, Pierre-Yves; Brizzi, Agostino; Huppertz, Berthold

doi:10.1016/j.jri.2023.104161

Cited by 1 publication

(2 citation statements)

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“…Interestingly, a recent transcriptomic analysis using microarrays revealed that among the 34 expressed proteoglycans in the placenta, syndecan-1 (SDC1) production is significantly the highest, and SDC1 is the most upregulated gene during the differentiation of trophoblast into syncytiotrophoblast ( 198 ). This suggests the existence of a pregnancy-specific glycocalyx that distinguishes itself from the glycocalyx of both adult and fetal endothelium and whose balance could contribute to the successful progression of pregnancy ( 199 ).…”

Section: Endothelium In Pregnancymentioning

confidence: 99%

“…The placenta is a physiological immunological niche, especially under the influence of physiological hypoxia that contributes to immunological regulation ( 209 ). However, placental hypoxia has others consequences as the generation of oxidative stress and trophoblastic secretion of sFLT-1, promoting antiangiogenic activities and endothelial injury ( 210 ), alteration in placental metabolism favoring interruption of the glycocalyx susceptible to contribute to localized complement activation ( 199 , 211 , 212 ). Thus, a pathological placental hypoxia, as observed in the case of PE, represents a risk situation for TMA.…”

Section: Endothelium In Pregnancymentioning

confidence: 99%

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Pregnancy as a susceptible state for thrombotic microangiopathies

Frimat,

Gnemmi,

Stichelbout

et al. 2024

Front. Med.

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Pregnancy and the postpartum period represent phases of heightened vulnerability to thrombotic microangiopathies (TMAs), as evidenced by distinct patterns of pregnancy-specific TMAs (e.g., preeclampsia, HELLP syndrome), as well as a higher incidence of nonspecific TMAs, such as thrombotic thrombocytopenic purpura or hemolytic uremic syndrome, during pregnancy. Significant strides have been taken in understanding the underlying mechanisms of these disorders in the past 40 years. This progress has involved the identification of pivotal factors contributing to TMAs, such as the complement system, ADAMTS13, and the soluble VEGF receptor Flt1. Regardless of the specific causal factor (which is not generally unique in relation to the usual multifactorial origin of TMAs), the endothelial cell stands as a central player in the pathophysiology of TMAs. Pregnancy has a major impact on the physiology of the endothelium. Besides to the development of placenta and its vascular consequences, pregnancy modifies the characteristics of the women’s microvascular endothelium and tends to render it more prone to thrombosis. This review aims to delineate the distinct features of pregnancy-related TMAs and explore the contributing mechanisms that lead to this increased susceptibility, particularly influenced by the “gravid endothelium.” Furthermore, we will discuss the potential contribution of histopathological studies in facilitating the etiological diagnosis of pregnancy-related TMAs.

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Section: Endothelium In Pregnancymentioning

confidence: 99%