bims-placeb 2026-02-22 papers

bims-placeb

Biomed News

on Placental cell biology

Issue of 2026–02–22
twelve papers selected by
Carlos M Guardia, National Institute of Environmental Health Sciences

Toxoplasma gondii infection misdirects placental trophoblast lineage specification.
An epigenetic blueprint for placental syncytiotrophoblast development.
Linking Oxidative Stress to Placental Dysfunction: The Key Role of Mitochondria in Trophoblast Function.
Metabolic imprinting in trophoblast barrier dysfunction: the role of glucolipotoxicity, endoplasmic reticulum stress, and amino acid transport imbalance.
The placental tryptophan pathway across gestation: implications for pregnancy outcomes.
Dll4 assembles the umbilical cord and placental vasculature.
Placental iron utilisation in fetal growth restriction: alterations in mitochondrial haem synthesis and iron-sulphur cluster assembly pathways.
Extracellular Vesicles and the Placenta-Brain Axis: Mechanisms of Shared Risk in Pregnancy and Perinatal Psychiatry.
Perfluoroalkyl and polyfluoroalkyl substances (PFAS) in trace levels via drinking water diminishes mouse embryo mitochondria function across three generations.
In Vitro 3D Model of Human Endometrial Stromal and Trophoblast Cells: Techniques for an Optimized Formation and Cryopreservation of Spheroids.
Aging mothers, failing placentas? Association between maternal age and placental perfusion in a low-resource setting.
Pathophysiologic mechanisms and molecular targets in preeclampsia.

Cell Rep. 2026 Feb 12. pii: S2211-1247(25)01597-9. [Epub ahead of print]45(2): 116825

Toxoplasma gondii infection misdirects placental trophoblast lineage specification.

Leah F Cabo, Liheng Yang, Mingze Gao, Rafaela J da Silva, NyJaee N Washington, Sarah M Reilly, Christina J Megli, Carolyn B Coyne, Jon P Boyle.

  Pregnancy is a critical point of vulnerability to pathogen infection. The placenta is a protective and nutrient-permeable barrier to most infectious agents, but a few can bypass its defenses. Little is known about how exposure to these pathogens impacts ongoing placental development. We demonstrate that Toxoplasma gondii misdirects the developmental program of trophoblast stem cells. Infection of progenitor cytotrophoblasts prevents fusion and differentiation to syncytiotrophoblast. Rather, T. gondii elicits a unique transcriptional identity that polarizes cytotrophoblasts toward the extravillous trophoblast fate. Strong evidence of developmental disruption is found in orthogonal models, including trophoblast stem cells, trophoblast organoids, and chorionic villi. Manipulation of cell fate by the parasite is most dramatic in trophoblast organoids, where we see outgrowth of human leukocyte antigen G (HLA-G)-positive extravillous trophoblasts. Collectively, these data show that Toxoplasma antagonizes differentiation of an infection-resistant cell type by inducing formation of an infection-permissive cell type, therefore potentiating its own fetal transmission.

Keywords:  CP: developmental biology; CP: microbiology; Toxoplasma gondii; cell differentiation; congenital infection; cytotrophoblast; epithelial-to mesenchymal transition; extravillous trophoblast; placenta; syncytiotrophoblast; trophoblast

DOI:  https://doi.org/10.1016/j.celrep.2025.116825
Placenta. 2026 Feb 10. pii: S0143-4004(26)00050-0. [Epub ahead of print]

An epigenetic blueprint for placental syncytiotrophoblast development.

Stephen J Renaud.

  The placenta establishes a continuous epithelial barrier that separates maternal and fetal blood. The cell type lining this barrier is the syncytiotrophoblast (STB), an exceptional lineage comprising innumerable nuclei enclosed within a single uninterrupted cytoplasm. The STB mediates nutrient and gas exchange between maternal and fetal circulations and performs vital endocrine functions that modify maternal physiology to sustain pregnancy and support fetal growth. Maintenance of STB integrity is therefore critical for pregnancy success, and dysregulation of its formation and function is implicated in several severe pregnancy complications. As a postmitotic cell layer, STB expansion and renewal depend on underlying cytotrophoblasts exiting their progenitor state and fusing into the syncytium. Consequently, the STB contains nuclei and organelles of diverse ages, maturation states, and potentially distinct functions. Recent findings reveal substantial heterogeneity within STB nuclei, encompassing differences in transcriptional activity and chromatin organization. These variations may reflect nuclear age but could also represent an additional layer of transcriptional and epigenetic regulation required for syncytial function and stability. This review provides an overview of STB development and function, emphasizing epigenetic mechanisms that contribute to the structural and functional diversity of STB nuclei. Key gaps in knowledge are highlighted, including how nuclei interact and whether they can dynamically respond to changes in their local environment. Resolving these and other outstanding questions will advance our understanding of STB development, placental biology, and the pathophysiology of pregnancy complications.

Keywords:  Cytotrophoblast; Differentiation; Epigenetics; Fusion; Placenta; Syncytiotrophoblast

DOI:  https://doi.org/10.1016/j.placenta.2026.02.003
Med Sci (Basel). 2026 Jan 21. pii: 53. [Epub ahead of print]14(1):

Linking Oxidative Stress to Placental Dysfunction: The Key Role of Mitochondria in Trophoblast Function.

Ioanna Vasilaki, Anastasios Potiris, Efthalia Moustakli, Despoina Mavrogianni, Nikoletta Daponte, Theodoros Karampitsakos, Alexios Kozonis, Konstantinos Louis, Christina Messini, Themos Grigoriadis, Ekaterini Domali, Sofoklis Stavros.

  Oxidative stress (OS) is a critical regulator of placental development; however, its specific effects on trophoblast biology remain incompletely elucidated. This narrative review synthesizes evidence derived from studies using human placental tissues and trophoblast cell models to delineate how excessive reactive oxygen species (ROS) disrupt molecular and cellular pathways essential for normal placentation. The literature search was restricted to human-based and in vitro investigations. Across these studies, OS was consistently shown to impair mitochondrial function in trophoblasts, resulting in increased mitochondrial ROS generation, loss of mitochondrial membrane potential, and activation of apoptotic signaling cascades. These mitochondrial disturbances were associated with reduced trophoblast proliferation, migration, and invasion, as well as dysregulation of angiogenic balance. Furthermore, several studies reported alterations in mitophagy, involvement of redox-sensitive pathways such as CYP1A1 and KLF9, and the extracellular release of mitochondrial DNA, which was linked to reduced cell viability and increased necrotic cell death. Collectively, the available evidence indicates that OS interferes with key trophoblast-dependent developmental processes, providing mechanistic insight into the pathogenesis of placental dysfunction observed in pregnancy complications such as preeclampsia (PE) and intrauterine growth restriction (IUGR). Elucidation of these pathways may inform the development of targeted therapeutic strategies aimed at preserving placental function and improving adverse pregnancy outcomes.

Keywords:  mitochondrial dysfunction; oxidative stress (OS); pregnancy complications; reactive oxygen species (ROS); redox homeostasis; trophoblast dysfunction

DOI:  https://doi.org/10.3390/medsci14010053
J Assist Reprod Genet. 2026 Feb 16.

Metabolic imprinting in trophoblast barrier dysfunction: the role of glucolipotoxicity, endoplasmic reticulum stress, and amino acid transport imbalance.

Shuo Zhang, Zi Xuan Shen, Pin Cao, Sha Ni, Dan Wang.

  The syncytiotrophoblast is central to maternal-fetal exchange and endocrine regulation, with its barrier integrity ensuring nutrient supply, immune defense, and metabolic balance. Maternal metabolic disturbances induce metabolic imprinting, whereby epigenetically regulated imprinted genes alter trophoblast physiology, nutrient transport, and growth signaling. Aberrant imprinting amplifies oxidative, inflammatory, and endoplasmic reticulum stress, impairing trophoblast differentiation, fusion, and hormone synthesis. A salient outcome is disruption of amino acid transport and the mechanistic target of rapamycin (mTOR) signaling, restricting fetal nutrient delivery and promoting growth restriction. This review synthesizes current evidence linking metabolic imprinting, stress responses, and transporter dysfunction as a multifactorial basis for syncytiotrophoblast failure and pregnancy complications. Further discussions on emerging stress-related biomarkers and potential therapeutic strategies, including antioxidants, metabolic modulators, and nutritional interventions, to restore placental efficiency. Metabolic imprinting establishes a pathological memory within the placenta, rendering it vulnerable to maternal metabolic insults and predisposing offspring to long-term metabolic disorders. Targeting these interconnected pathways may offer early opportunities for intervention and improved pregnancy outcomes.

Keywords:  Amino acid transport; Endoplasmic reticulum stress; Glucolipotoxicity; Metabolic imprinting; Placenta; Trophoblast

DOI:  https://doi.org/10.1007/s10815-026-03830-4
Hum Reprod Update. 2026 Feb 19. pii: dmag001. [Epub ahead of print]

The placental tryptophan pathway across gestation: implications for pregnancy outcomes.

Rona Karahoda, David Walker, Cilia Abad, Kasin Yadunandam Anandam, Padma Murthi, Frantisek Staud.

   BACKGROUND: Tryptophan metabolism within the placenta generates bioactive metabolites, including serotonin (5-hydroxytryptamine; 5-HT), melatonin, and kynurenine derivatives, that regulate immune tolerance, vascular function, oxidative balance, and fetal neurodevelopment. Increasing evidence indicates that placental handling of tryptophan is dynamically regulated across gestation and is highly sensitive to maternal environmental and metabolic cues.
OBJECTIVE AND RATIONALE: The aim of this review is to examine placental tryptophan metabolism across gestation, with a focus on the 5-HT, melatonin, and kynurenine pathways. We address how these pathways are regulated during normal pregnancy and how maternal factors, including inflammation, hypoxia, oxidative stress, and cardiometabolic dysfunction, influence placental tryptophan handling in pregnancy complications such as early pregnancy loss, preeclampsia, fetal growth restriction, and preterm birth.
SEARCH METHODS: PubMed was searched using predefined terms related to placental tryptophan metabolism, 5-HT, melatonin, kynurenine, fetal programming, neurodevelopment, and pregnancy complications. Only full-text, peer-reviewed articles published in English were included. Abstracts and conference proceedings were excluded due to their limited data reliability.
OUTCOMES: Placental tryptophan metabolism shows clear gestational stage-dependent regulation, and early pregnancy emerges as a formative period when pathway activity and metabolite balance are first established. From early pregnancy, maternal-decidual kynurenine pathway activity and placental 5-HT synthesis intersect with immune tolerance, vascular adaptation, and neurodevelopmental signaling. Across gestation, maternal inflammation, hypoxia, oxidative stress, and cardiometabolic disturbance can redirect the tryptophan flux and shift the balance between 5-HT/melatonin and downstream kynurenine metabolites. Evidence across pregnancy complications links early pathway disruption to pregnancy loss and supports the view that early metabolic perturbations contribute to vulnerability for later placental dysfunction, including preeclampsia, fetal growth restriction, and preterm birth.
WIDER IMPLICATIONS: Placental tryptophan metabolism changes across gestation, making early pregnancy a critical window when pathway balance and fetal exposure to neuroactive metabolites are first set. Maternal inflammation, metabolic status, nutrition, and drug exposures may alter this balance, with the placenta acting as the key interface that transmits maternal signals to the fetus and shapes neurodevelopmental trajectories. To define the clinical relevance of altered tryptophan catabolism, longitudinal human studies are needed to link placental phenotypes with pregnancy outcomes and postnatal neurodevelopment. These should be complemented by mechanistic models that resolve regulation in early gestation.
REGISTRATION NUMBER: n/a.

Keywords:  DOHaD; fetal programming; kynurenine; melatonin; neurodevelopment; placenta; serotonin; tryptophan metabolism

DOI:  https://doi.org/10.1093/humupd/dmag001
JCI Insight. 2026 Feb 17. pii: e194461. [Epub ahead of print]

Dll4 assembles the umbilical cord and placental vasculature.

Derek C Sung, Hana A Ahanger, Sweta Narayan, Jesse A Pace, Mei Chen, Jisheng Yang, Siqi Gao, T C S Keller Iv, Jenna Bockman, Xiaowen Chen, Erica Nguyen, Alan T Tang, Patricia Mericko-Ishizuka, Ivan Maillard, Mark L Kahn.

  Proper development of the umbilical cord and placental vasculature is essential for embryonic development. While the allantois is known give rise to endothelial cells (ECs) within the placenta, whether the allantois gives rise to ECs in the umbilical cord is debated. Furthermore, a lack of genetic tools to study placental vascular development independent of the embryo proper has hindered robust investigation into the primary cause of vascular defects from early studies utilizing global knockouts. In this study, we delineate the contribution of the allantois to the umbilical vessels and utilize a mouse genetic tool previously developed by our lab to revisit the role of Notch signaling during placental development. We show that the allantois has mosaic contribution to the umbilical endothelium with higher contributions closer to the placenta. Allantoic deletion of Dll4 disrupts umbilical cord and placental vascular formation with secondary defects in the heart. Lastly, we identify Unc5b downstream of Notch signaling that restricts EC migration while promoting chemokine signaling for smooth muscle cell (SMC) recruitment to arteries. These findings identify a genetic tool for investigating placental vascular development and give new insights into the ontogeny and mechanisms of placental vascular and umbilical cord development.

Keywords:  Angiogenesis; Development; Endothelial cells; Reproductive biology; Vascular biology

DOI:  https://doi.org/10.1172/jci.insight.194461
J Physiol. 2026 Feb 16.

Placental iron utilisation in fetal growth restriction: alterations in mitochondrial haem synthesis and iron-sulphur cluster assembly pathways.

Veronica B Botha, Heather C Murray, Siddharth Acharya, Kirsty G Pringle, Roger Smith, Joshua J Fisher.

  Fetal growth restriction (FGR) affects ∼10% of pregnancies worldwide and is often associated with placental insufficiency. Iron is essential for maternal haematopoietic adaptations and placental processes such as mitochondrial iron-sulphur (Fe-S) cluster assembly, haem synthesis and erythropoiesis. This study aimed to characterise iron transport and downstream utilisation in FGR. Placental tissues from term uncomplicated (n = 19) and FGR (n = 18) pregnancies were analysed. Maternal iron status was retrospectively assessed from clinical records. Placental mRNA and protein expression of iron-dependent pathways were analysed via RT-qPCR, LC-MS and western blotting. Placental iron content was assessed histologically, and haem levels were measured by an activity assay. FGR pregnancies showed significantly elevated maternal serum ferritin and lower red cell distribution width, although these remained within normal clinical values. Placental iron uptake transporters TFRC and DMT1 were significantly upregulated, while the iron exporter to the fetus, ferroportin, was reduced, indicating increased iron retention in the FGR placenta. Despite altered transporter expression, Fe3 + iron levels were unchanged, suggesting iron utilisation over storage. Subsequent investigations identified reduced mitochondrial Fe-S synthesis components (FDXR, FDX2, NDUFAB1, HSPA9), and a prioritisation of mitochondrial and cytosolic haem synthesis enzymes in FGR. Protein levels of haemoglobin subunits (HBG1, HBG2, HBB, HBA1) and erythrocyte membrane markers (EPB41, EPB42, SPTA1, SPTB, ANK1) were decreased. These findings reveal a compensatory response in FGR placentae, with increased iron uptake and utilisation favouring haem synthesis over Fe-S cluster formation, possibly to support oxygen handling under poor placental vascularisation and reduced fetal oxygenation, with potential consequences for mitochondrial energy metabolism. KEY POINTS: Iron plays a critical role in placental function, and while iron-dependent pathway components are well-characterised, their integrated response and adaptive reprogramming in fetal growth restriction (FGR) remain poorly understood. In FGR, maternal iron status was unchanged, however, placental iron uptake proteins were increased and ferroportin reduced, suggesting that the placenta retains iron. FGR placentae showed altered de novo mitochondrial iron-sulphur cluster (Fe-S) formation and a bottleneck in late-stage Fe-S cluster assembly. This shift in Fe-S synthesis prioritises mitochondrial and cytosolic haem synthesis pathways, consistent with increased haem utilisation and breakdown. Globin subunits were lower in protein abundance and impaired placental erythrocyte structure in FGR. Dysregulation of erythrocyte membrane proteins in FGR placentae suggests altered erythrocyte structure, potentially representing an adaptive response to inadequate vascularisation, attempting to optimise oxygen delivery to the fetus.

Keywords:  erythrocyte structure; fetal growth restriction; haem synthesis; iron transport; iron–sulphur clusters; mitochondria; placenta

DOI:  https://doi.org/10.1113/JP289451
Curr Opin Physiol. 2026 Mar;pii: 100913. [Epub ahead of print]47

Extracellular Vesicles and the Placenta-Brain Axis: Mechanisms of Shared Risk in Pregnancy and Perinatal Psychiatry.

Hannah Hazzard, Brianna Blaine, Benjamin B Borrman, Susan Qi Shen, Serena Banu Gumusoglu.

  Disorders of pregnancy and psychiatric conditions in mothers and affected children have high rates of comorbidity and underlying mechanistic overlap. We propose that extracellular vesicles (EVs) may subserve this shared psycho-obstetric risk. EVs are small lipid bilayer-bound particles containing regulatory nucleic acids and proteins that are released from cells into circulation, where they readily cross blood-brain and placental barriers. In pregnancy, EVs are produced in large numbers by the placenta and have been implicated in pregnancy-related medical and psychiatric conditions via vascular, endocrine, and immune mechanisms.

Keywords:  Extracellular vesicles; endocrine signaling; obstetrics; placenta; pregnancy; psychiatry

DOI:  https://doi.org/10.1016/j.cophys.2026.100913
Environ Res. 2026 Feb 14. pii: S0013-9351(26)00371-3. [Epub ahead of print]296 124043

Perfluoroalkyl and polyfluoroalkyl substances (PFAS) in trace levels via drinking water diminishes mouse embryo mitochondria function across three generations.

Yasmyn E Winstanley, Donna L Holland, Nicole O McPherson, Erin Barrera, Haley S Connaughton, Darryl L Russell, Sarah A Robertson, Cameron J Shearer, Rebecca L Robker.

  Perfluoroalkyl and polyfluoroalkyl substances (PFAS), synthetic and resistant to degradation, are present at trace levels in municipal drinking water. PFAS exposure is associated with female infertility and developmental anomalies, yet how these compounds influence ovarian function and embryogenesis is not understood. Thus, the impact of exposure to PFAS via drinking water on oocyte viability and embryo development was examined. The local tap water was found to contain ∼3 ng/L PFAS, primarily PFOS, PFOA, and PFHxS. Female mice were then given purified water containing 5 ng/L or 50 ng/L of these same three PFAS compounds or drinking fountain (tap) water for 4 weeks or 6 months. Ovulation, oocyte quality, embryo development and fetal weight were analyzed across three generations. Embryos from PFAS-exposed females (5 ng/L or 50 ng/L PFAS or tap water) exhibited impaired mitochondrial function, DNA damage and fewer cells, and reduced fetal weight. Embryo phenotypes were similar whether females were PFAS-exposed for 4 weeks, 6 months or just the first 4 weeks of the 6 months. Offspring drank purified water, yet fertility analysis showed similar embryonic and neonatal phenotypes in the F1 'daughters' of the PFAS-exposed females, and in the embryos of F2 females ('granddaughters' of PFAS-exposed females). To determine causality and whether defects are reversible, embryos were treated mitochondria-modulating compounds, with responses indicating that PFAS exposure irreversibly impairs key aspects of mitochondrial function. These findings identify cellular targets and mechanisms by which PFAS disrupt female fertility; reveal that PFAS cause intergenerational changes in mammalian embryos; and have important implications for water quality policies.

Keywords:  Drinking water; Embryo; Female fertility; Mitochondria; Oocyte; PFAS

DOI:  https://doi.org/10.1016/j.envres.2026.124043
Methods Protoc. 2026 Feb 13. pii: 27. [Epub ahead of print]9(1):

In Vitro 3D Model of Human Endometrial Stromal and Trophoblast Cells: Techniques for an Optimized Formation and Cryopreservation of Spheroids.

Karthika Muthuraj, Iwona Scheliga, Dunja M Baston-Buest, Jana Bender-Liebenthron, Jan-Steffen Kruessel, Alexandra P Bielfeld.

  Three-dimensional (3D) cell culture models provide physiologically relevant systems that mimic the native endometrial environment better than 2D models and offer reliable platforms to study embryo implantation and maternal-embryo interactions. One widely used 3D culture model is the generation of spheroids. However, standardized and reproducible methods for generating uniform spheroids from trophoblast and endometrial stromal cells are limited. In this study, we established and validated a robust protocol for spheroid formation using human trophoblast (HTR8/SVneo, JEG3) and endometrial stromal (St-T1b, tHESC) cell lines. The protocol was further extended to generate spheroids from decidualized tHESC, representing a novel approach that closely reflects the receptive endometrial environment. Key parameters, including cell concentration and methyl cellulose supplementation, were optimized to produce compact and homogeneous spheroids. Spheroid formation was monitored at defined intervals (0, 8, 24, 32, and 48 h), and decidualized spheroids were assessed up to 72 h. Long-term cryopreservation over 11 months demonstrated high post-thaw viability across all spheroid types, as confirmed by Calcein-AM staining. This standardized workflow provides a reliable 3D model incorporating hormonally primed stromal cells and offers a practical platform to investigate the mechanisms underlying normal and trophoblast invasion in vitro.

Keywords:  3D spheroid model; decidualized spheroids; freezing of spheroids; methyl cellulose; post-thaw viability

DOI:  https://doi.org/10.3390/mps9010027
PLOS Glob Public Health. 2026 ;6(2): e0005943

Aging mothers, failing placentas? Association between maternal age and placental perfusion in a low-resource setting.

Innocent Okafor Eze, Uchenna Ifeanyi Nwagha, Stephen Chijioke Eze, Asma'u Eleojo Abdul, Victor Cletus Igboezue, Rufai Muhammed.

The prevalence of pregnancies among women of advanced maternal age (AMA, ≥ 35 years) is increasing globally. Age-related vascular changes may influence placental perfusion, but evidence isolating maternal age from major confounders remains limited, particularly in low-resource settings. The objective of the study was to examine the association between maternal age and placental vascular resistance, measured using the umbilical artery pulsatility index (UA-PI). This prospective cross-sectional comparative study was conducted at a tertiary military hospital in Lagos, Nigeria. One hundred pregnancies at term were stratified into younger maternal age (<35 years, n = 50) and AMA (≥35 years, n = 50) groups. Umbilical artery Doppler assessments were performed at 37 weeks' gestation. Mean UA-PI values were compared across maternal age groups using one-way analysis of variance with Tukey post hoc testing. Effect sizes are presented with 95% confidence intervals. At 37 weeks' gestation, mean UA-PI was higher among women with AMA compared with younger women (0.98 ± 0.20 vs 0.80 ± 0.19; mean difference 0.18, 95% CI 0.08-0.28; p = 0.001). A progressive increase in UA-PI was observed across age categories (<25, 25-34, 35-40, ≥ 41 years; p = 0.006). Advanced maternal age was associated with higher umbilical artery vascular resistance in this cohort. These findings support further evaluation of Doppler-based placental surveillance strategies for AMA pregnancies, particularly in low-resource settings.

DOI: https://doi.org/10.1371/journal.pgph.0005943
Clin Chim Acta. 2026 Feb 14. pii: S0009-8981(26)00067-7. [Epub ahead of print] 120885

Pathophysiologic mechanisms and molecular targets in preeclampsia.

Jinxuan Ren, Mei Yang, Qing Zhu, Menghui Wang, Nanfang Li.

  Preeclampsia is a pregnancy-specific multisystem disorder. With a global incidence of 2%-8%, preeclampsia is a major contributor to maternal and neonatal morbidity and mortality. The pathogenesis of preeclampsia is commonly described by a two-stage model. The first stage involves defective placentation in early pregnancy, marked by insufficient extravillous trophoblast invasion, impaired spiral artery remodeling, dysregulated sphingolipid metabolism, and an imbalance in immune tolerance; these anomalies lead to placental ischemia and hypoxia. The second stage consists of systemic maternal responses in the mid-to-late gestation period, including angiogenic imbalance, systemic inflammation, and endothelial dysfunction, which manifest as the clinical symptoms. Recent advances in multi-omics technologies and liquid biopsy have accelerated the discovery of novel biomarkers enabling non-invasive early prediction. Emerging therapeutic strategies target key pathological pathways: low-molecular-weight heparin to restore angiogenic balance and reduce inflammation, complement system inhibitors to counter aberrant activation, and epigenetic modulators to ameliorate endothelial dysfunction. Despite this progress, significant challenges remain, including the heterogeneity of preeclampsia, limited clinical validation of biomarkers and therapeutic targets, and the management of long-term cardiovascular sequelae. Future research should prioritize developing precision prediction models, conducting large-scale clinical trials for targeted therapies, and establishing comprehensive postpartum follow-up systems to improve the prevention, diagnosis, and treatment of preeclampsia.

Keywords:  Biomarkers; Pathologic processes; Prediction; Preeclampsia; Therapeutics

DOI:  https://doi.org/10.1016/j.cca.2026.120885