ReviewFrontiers in endocrinology2023
Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction.
Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 47 citations in OpenAlex.
- IsGut microbes · 2026Review
- Trophoblast metabolic reprogramming triggers adverse pregnancy outcomes during DENV-2 infection in mice.Journal of virology · 2026Article
- Maternal hyperhomocysteinemia promotes adverse pregnancy outcomes via mtDNA-cGAS-STING signaling-mediated trophoblast mitophagy.Redox biology · 2026Article
- IGF-1Eb Isoform Immunoreactivity May Be Associated with Placental Dysfunction and Vascular Pathology in Fetal Growth Restriction (FGR).Biomolecules · 2026Article
- Evolutionary co-option of endogenous retroviruses: syncytins as regulators of placental development and disease.Molecular biology reports · 2026Review
- Characterizing glial cells missing transcription factor 1 (GCM1)'s role in regulating placental gene expression.Placenta · 2026Article
- Placental dysfunction reflects endocrine impairment and trophoblast alterations in polycystic ovarian syndrome.Scientific reports · 2026Article
- Breaking cellular boundaries: molecular mechanisms of tunneling nanotube formation and fusion.Biochemical Society transactions · 2026Review
- Gestational fine particulate matter exposure and perinatal outcomes in the ECHO cohort: Associations across pregnancy windows.Environmental research · 2026Article
- The dual face of human chorionic gonadotropin in the CNS: neuroprotection, signaling, and possible pathological effects.Archives of gynecology and obstetrics · 2026Review
- Article
- Integrative Analysis of Placental Methylomes Identifies Epigenetically Regulated Genes Implicated in Fetal Growth Restriction.International journal of molecular sciences · 2026Article
- Shedding light on the function of autophagy in complicated pregnancies.Cell death & disease · 2026Review
- Efficacy of Normobaric High-Flow Oxygen Therapy Combined with Low Molecular Weight Heparin in the Management of Fetal Growth Restriction: A Prospective Cohort Study.International journal of women's health · 2026Article
- Co-trimoxazole-induced reproductive toxicity and placental-barrier disruption: impact on cell-cell junctions and ERK signaling pathway.Frontiers in cell and developmental biology · 2026Article
- The placental maturation inflection point: an integrative biological framework for understanding early-onset versus late-onset preeclampsia.Frontiers in endocrinology · 2026Review
- The placental transcriptome serves as a mechanistic link between prenatal phthalate exposure and placental efficiency.Environment international · 2025Article
- Analysis of prenatal medication use and placental epigenetic gestational age in extremely low gestational age newborns (ELGANs) highlight relationships to aspirin use during pregnancy.Clinical epigenetics · 2025Article
- BHLHE40 Cooperates with GATA2/3 to Control Human Syncytiotrophoblast Lineage Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular Insights into Human Placentation: From Villous Morphogenesis to Pathological Pathways and Translational Biomarkers.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Placental dysfunction refers to the insufficiency of placental perfusion and chronic hypoxia during early pregnancy, which impairs placental function and causes inadequate supply of oxygen and nutrients to the fetus, affecting fetal development and health. Fetal intrauterine growth restriction, one of the most common outcomes of pregnancy-induced hypertensions, can be caused by placental dysfunction, resulting from deficient trophoblast syncytialization, inadequate trophoblast invasion and impaired vascular remodeling. During placental development, cytotrophoblasts fuse to form a multinucleated syncytia barrier, which supplies oxygen and nutrients to meet the metabolic demands for fetal growth. A reduction in the cell fusion index and the number of nuclei in the syncytiotrophoblast are found in the placentas of pregnancies complicated by IUGR, suggesting that the occurrence of IUGR may be related to inadequate trophoblast syncytialization. During the multiple processes of trophoblasts syncytialization, specific proteins and several signaling pathways are involved in coordinating these events and regulating placental function. In addition, epigenetic modifications, cell metabolism, senescence, and autophagy are also involved. Study findings have indicated several abnormally expressed syncytialization-related proteins and signaling pathways in the placentas of pregnancies complicated by IUGR, suggesting that these elements may play a crucial role in the occurrence of IUGR. In this review, we discuss the regulators of trophoblast syncytialization and their abnormal expression in the placentas of pregnancies complicated by IUGR.
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