Fetal microchimerism and the two-stage model of preeclampsia

Jacobsen, Daniel Pitz; Fjeldstad, Heidi Elisabeth; Sugulle, Meryam; Johnsen, Guro M.; Olsen, Maria Belland; Kanaan, Sami B; Staff, Anne Cathrine

doi:10.1016/j.jri.2023.104124

Cited by 2 publications

(1 citation statement)

References 96 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the growing placenta toward term, and in large placentas in general, the restricted placental capacity as described in the The two-stage model of preeclampsia, including effects of cellular senescence. This figure is further developed from our prior published papers [3,14,15,129]. Stage 1 is characterized by placental dysfunction a result of syncytiotrophoblast stress, leading to the excessive release of proinflammatory factors into the maternal circulation.…”

Section: Type B Placenta (Intrinsic) Problem (Figure 1): Placental Ca...mentioning

confidence: 99%

Placental Senescence and the Two‐Stage Model of Preeclampsia

Sugulle,

Fiskå,

Jacobsen

et al. 2024

American J Rep Immunol

Self Cite

View full text Add to dashboard Cite

In this review, we summarize how an increasingly stressed and aging placenta contributes to the maternal clinical signs of preeclampsia, a potentially lethal pregnancy complication. The pathophysiology of preeclampsia has been conceptualized in the two‐stage model. Originally, highlighting the importance of poor placentation for early‐onset preeclampsia, the revised two‐stage model explains late‐onset preeclampsia as well, which is often preceded by normal placentation. We discuss how cellular senescence in the placenta may fit with the framework of the revised two‐stage model of preeclampsia pathophysiology and summarize potential cellular and molecular mechanisms, including effects on placental and maternal endothelial function. Cellular senescence may occur in response to inflammatory processes and oxidative, mitochondrial, or endoplasmic reticulum stress and chronic stress induce accelerated, premature placental senescence. In preeclampsia, both circulating and tissue‐based senescence markers are present. We suggest that aspirin prophylaxis, commonly recommended from the first trimester onward for women at risk of preeclampsia, may affect placentation and possibly mechanisms of placental senescence, thus attenuating the risk of preeclampsia developing clinically. We propose that biomarkers of placental dysfunction and senescence may contribute to altered preventive strategies, including discontinuation of aspirin at week 24–28 depending on placenta‐associated biomarker risk stratification.

show abstract

Section: Type B Placenta (Intrinsic) Problem (Figure 1): Placental Ca...mentioning

confidence: 99%