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Molecular Pathology of the Placenta in Pregnancy Complications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 93

Special Issue Editors


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Guest Editor
1. Capio Specialized Center for Gynecology, Postgången 53, 171 45 Solna, Sweden
2. Department of Obstetrics and Gynecology, University of Szeged, H-6725 Szeged, Hungary
Interests: molecular, ultrasound and clinical characterization of pregnancy complications; placental histology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, University of Szeged, H-6725 Szeged, Hungary
Interests: perinatal ultrasound; serum markers for complications of pregnancy; histopathology of the placenta; neonatal pathological conditions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Trophoblast invasion is essential in early pregnancy for remodeling maternal spiral arteries and ensuring adequate placental blood flow to support fetal development. This process involves three trophoblast subtypes: syncytiotrophoblast, responsible for nutrient exchange and hormone secretion; cytotrophoblast, which acts as a proliferative progenitor; and extravillous trophoblast, which invades maternal tissue and remodels vasculature. Dysregulated trophoblast invasion is linked to pregnancy complications such as preeclampsia, intrauterine growth restriction, gestational diabetes mellitus (GDM), and hypertensive disorders. Several maternal serum biomarkers reflect placental function, including placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), pregnancy-associated plasma protein A (PAPP-A) and human chorionic gonadotropin (hCG), as well as endoglin and laeverin. Endoglin, a TGF-β co-receptor, is key in angiogenesis, while laeverin, expressed by extravillous trophoblasts, aids invasion. Despite this, many placental proteins and molecular factors—such as inflammatory cytokines (TNF-α, IL-6), angiogenic modulators (angiopoietins), extracellular matrix proteins, and oxidative stress markers—are underexplored in maternal serum. Environmental factors like hypoxia, metabolic status, immune interactions, epigenetic regulation, and signaling pathways (Notch, Wnt, TGF-β) also affect trophoblast function. The limited profiling of these molecules presents a research gap in early prediction of complications like GDM and hypertensive disorders. New insights addressing these gaps are awaited to enhance biomarker discovery, diagnosis, and therapeutic strategies for improved maternal-fetal outcomes. This Special Issue also focuses on new technical tools in this field: organoids/assembloids, spatial transcriptomics, spatial proteomics, single-cell epigenomics/transcriptomics and targeted delivery to the placenta.

We look forward to receiving your contributions.

Dr. Zoltan Kozinszky
Dr. Andrea Suranyi
Guest Editors

Manuscript Submission Information

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Keywords

  • pregnancy complications
  • placental histology
  • biomarker
  • trophoblast invasion
  • molecular diagnostics and therapeutics

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Published Papers (1 paper)

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Research

13 pages, 1956 KiB  
Article
Differential Immune Checkpoint Expression in CD4+ and CD4 NKT Cell Populations During Healthy Pregnancy
by Matyas Meggyes, Nagy U. David, Livia Mezosi, Fanni Vastag, Dora Kevey and Laszlo Szereday
Int. J. Mol. Sci. 2025, 26(16), 8022; https://doi.org/10.3390/ijms26168022 - 19 Aug 2025
Abstract
This study investigated the expression of immune checkpoint molecules on CD4+ and CD4 NKT cell subpopulations throughout healthy pregnancy trimesters and in non-pregnant condition to understand their role in maternal–fetal immunotolerance. Using flow cytometry, we found that CD4 NKT cells [...] Read more.
This study investigated the expression of immune checkpoint molecules on CD4+ and CD4 NKT cell subpopulations throughout healthy pregnancy trimesters and in non-pregnant condition to understand their role in maternal–fetal immunotolerance. Using flow cytometry, we found that CD4 NKT cells significantly outnumbered CD4+ NKT cells in all investigated groups. In the case of the immune checkpoint molecules, PD-1 receptor expression was significantly lower in CD4 NKT cells compared to CD4+ counterpart cells only in non-pregnant women, while the PD-L1 ligand expression on CD4+ NKT cells significantly decreased in the third trimester. In contrast, LAG-3 and Galectin-3 expressions remained stable across all subsets and trimesters. For the TIGIT/CD226 axis, CD226 expression was significantly higher in CD4+ NKT cells in the third trimester and in non-pregnant women. The two ligands CD112 and CD155 were consistently lower on CD4 NKT cells across all groups. The activating receptor NKG2D was significantly higher on CD4 NKT cells in all examined cohorts. These findings suggest that CD4+ NKT cells tend towards a more tolerogenic phenotype, while CD4 NKT cells maintain a balanced cytotoxic potential with reduced immunoregulation function. The dynamic regulation of immune checkpoints on NKT cell subsets, particularly the downregulation of PD-L1 and CD226 in late pregnancy, highlights their fine-tuned role in balancing maternal–fetal immune tolerance with readiness for parturition. Full article
(This article belongs to the Special Issue Molecular Pathology of the Placenta in Pregnancy Complications)
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