Preeclampsia and Fetal Congenital Heart Defects

Barros, Tânia; Ferreira, Bárbara D.; Moleiro, Maria Lúcia; Guedes-Martins, Luís

doi:10.2174/1573403x18666220415150943

Cited by 5 publications

(3 citation statements)

References 108 publications

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“…It is widely reported that abnormal angiogenesis in the placenta can lead to the development of not only FGR, but also maternal preeclampsia (PE) [ 2 ], due to impaired remodeling of maternal spiral arteries and placental under perfusion. However, in the last few years, various reports have suggested that placenta-related complications due to angiogenic imbalance may be associated with fetal cardiac remodeling and subclinical dysfunction [ 3 , 4 , 5 , 6 , 7 , 8 , 9 ], as well as a higher risk of congenital heart disease (CHD) [ 10 , 11 , 12 ]. These fetuses are then associated with poorer perinatal outcome, more prenatal death, severe intrapartum fetal distress, and perinatal brain injury [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Longitudinal Behavior of Left-Ventricular Strain in Fetal Growth Restriction

et al. 2023

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Fetal growth restriction (FGR) is associated with an increased risk of adverse outcomes resulting from adaptive cardiovascular changes in conditions of placental insufficiency, leading to cardiac deformation and dysfunction, which can be evaluated with 2D speckle tracking echocardiography (2D-STE). The aim of the present study was to evaluate whether reduced fetal growth is associated with cardiac left-ventricle (LV) dysfunction, using 2D-STE software widely used in postnatal echocardiography. A prospective longitudinal cohort study was performed, and global (GLO) and segmental LV longitudinal strain was measured offline and compared between FGR and appropriate-for-gestational-age (AGA) fetuses throughout gestation. All cases of FGR fetuses were paired 1:2 to AGA fetuses, and linear mixed model analysis was performed to compare behavior differences between groups throughout pregnancy. Our study shows LV fetal longitudinal strain in FGR and AGA fetuses differed upon diagnosis and behaved differently throughout gestation. FGR fetuses had lower LV strain values, both global and segmental, in comparison to AGA, suggesting subclinical cardiac dysfunction. Our study provides more data regarding fetal cardiac function in cases of placental dysfunction, as well as highlights the potential use of 2D-STE in the follow-up of cardiac function in these fetuses.

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Section: Introductionmentioning

confidence: 99%

Longitudinal Behavior of Left-Ventricular Strain in Fetal Growth Restriction

et al. 2023

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“…Maldevelopment of the placenta is linked with a variety of serious pregnancy complications (e.g., preeclampsia, fetal growth restriction) that cause maternal and fetal illness or death 11 . Interestingly, these pregnancy complications are also associated with a higher incidence of CHDs, suggesting the notion of a shared developmental trajectory between the placenta and nascent heart gaining recognition as the "placenta-heart axis" 2,12 .…”

Section: Introductionmentioning

confidence: 99%

Placental extracellular vesicles promote cardiomyocyte maturation and fetal heart development

Renaud

Jeyarajah

Patterson

et al. 2023

Preprint

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Congenital heart defects are leading causes of neonatal mortality and are often associated with placental abnormalities, but mechanisms are unknown. Herein, we investigated a potential signaling network connecting the placenta and nascent heart in mice. We found that fetal hearts exposed to media conditioned by placental tissue or differentiated wild-type trophoblast stem (TS) cells, but not undifferentiated TS cells, showed increased heart rate and epicardial cell outgrowth. This effect was not observed when hearts were exposed to media from TS cells lacking OVO-like 2, a transcription factor required for trophoblast differentiation and placental development. Trophoblasts released abundant extracellular vesicles into media. These vesicles contained microRNAs such as mmu-miR-1249-3p, which was sufficient to mediate cardio-promoting effects. Our findings provide a potential mechanism whereby the placenta communicates with the fetal heart to promote cardiac morphogenesis, and offers insight into the link between poor placentation and a higher incidence of heart defects.

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“…It is important to note that this condition often resolves completely within 12 weeks following childbirth [8,9]. A large body of epidemiological research suggests that placental defects are thought to be caused by abnormal immune reactions of the mother to invading trophoblast cells, and preeclampsia is associated with primiparity, partner change, and oocyte donation for assisted reproduction [10,11]. Although there is a wealth of literature supporting the immunological origins of preeclampsia, its specifc underlying biological mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Echinatin Inhibits Oxidative Stress and Inflammatory Processes in Trophoblast Cells by Inhibiting TLR4-MyD88-NF-κB Pathway in Preeclampsia

Deng,

Chen,

Zhang

et al. 2024

Journal of Clinical Pharmacy and Therapeutics

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Background. Preeclampsia (PE) is a common obstetric disorder hallmarked by impaired trophoblast invasion and a skew toward an inflammatory immune response. Echinatin, a flavonoid with established anti-inflammatory, antioxidant, and anticancer activities, may offer therapeutic benefits in PE. Our study aimed to investigate the effect of echinatin on preeclampsia in vitro and in vivo and to reveal the potential molecular mechanism of its action. Methods. Eighteen adult female Sprague Dawley rats were randomized into three experimental groups: a PE model group, a PE + echinatin treatment group, and a PE + echinatin treatment group with TLR4 overexpression. Placental tissue CK7 expression was assessed by immunohistochemistry. TUNEL immunofluorescence staining quantified placental cell apoptosis. Cell viability, proliferation, and migration were evaluated using cell counting kit-8, EdU incorporation, and Transwell assays, respectively. Oxidative stress parameters of malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured. Flow cytometry determined cell apoptosis and intracellular reactive oxygen species (ROS) levels. Western blotting evaluated the expression of proteins related to the TLR4-MyD88-NF-κB signaling pathway, and the concentrations of TNF-α, IL-6, and IL-18 were measured with ELISA kits. Results. Echinatin mitigated placental damage, reduced apoptosis, and increased CK7 expression. It significantly enhanced HTR-8/SVneo cell viability and migration. Echinatin also counteracted H2O2-induced ROS production and cell death in HTR-8/SVneo cells. Moreover, it inhibited the expression of proteins within the TLR4-MyD88-NF-κB signaling cascade. Overexpression of TLR4 negated echinatin’s protective effects. Conclusion. Echinatin exerts protective effects against oxidative stress and inflammation in PE by targeting the TLR4-MyD88-NF-κB pathway, suggesting its therapeutic potential for the management of preeclampsia.

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Preeclampsia and Fetal Congenital Heart Defects

Cited by 5 publications

References 108 publications

Longitudinal Behavior of Left-Ventricular Strain in Fetal Growth Restriction

Longitudinal Behavior of Left-Ventricular Strain in Fetal Growth Restriction

Placental extracellular vesicles promote cardiomyocyte maturation and fetal heart development

Echinatin Inhibits Oxidative Stress and Inflammatory Processes in Trophoblast Cells by Inhibiting TLR4-MyD88-NF-κB Pathway in Preeclampsia

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