ArticleScientific reports2022
Mitochondrial dysfunction-induced high hCG associated with development of fetal growth restriction and pre-eclampsia with fetal growth restriction.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Integrated multi-omics profiling of amniotic fluid identifies predictive biomarkers for fetal growth restriction trajectories.Annals of medicine · 2026Article
- Single-cell insights into trophoblast heterogeneity and adaptive dysfunction in selective fetal growth restriction.Communications biology · 2026Article
- The dual face of human chorionic gonadotropin in the CNS: neuroprotection, signaling, and possible pathological effects.Archives of gynecology and obstetrics · 2026Review
- Integrative bioinformatics analysis identifies placental senescence-associated signatures in early-onset preeclampsia.Frontiers in endocrinology · 2026Article
- Trophoblast-derived proteins and their effects on the pathogenesis of preeclampsia.Histology and histopathology · 2026Review
- Variations in blood levels of the anti-fusogenic endogenous retroviral protein suppressyn are associated with fetal growth outcome in preeclampsia.Scientific reports · 2025Article
- Placental mitochondrial calcium uniporter modulates offspring susceptibility to metabolic dysfunction.Molecular metabolism · 2025Article
- Molecular Insights into Human Placentation: From Villous Morphogenesis to Pathological Pathways and Translational Biomarkers.International journal of molecular sciences · 2025Review
- The Role of Placental Mitochondrial Dysfunction in Adverse Perinatal Outcomes: A Systematic Review.Journal of clinical medicine · 2025Review
- Relationship between increased maternal serum free human chorionic gonadotropin levels in the second trimester and adverse pregnancy outcomes: a retrospective cohort study.BMC women's health · 2024Article
- Mitochondrial quality control alterations and placenta-related disorders.Frontiers in physiology · 2024Review
- Potential Association of Gut Microbial Metabolism and Circulating mRNA Based on Multiomics Sequencing Analysis in Fetal Growth Restriction.Mediators of inflammation · 2024Article
- The Gut Microbiota of Pregnant Rats Alleviates Fetal Growth Restriction by Inhibiting the TLR9/MyD88 Pathway.Journal of microbiology and biotechnology · 2023Article
- Recent advances and new perspectives in mitochondrial dysfunction.Scientific reports · 2023Article
- Pathophysiological impact of CXC and CX3CL1 chemokines in preeclampsia and gestational diabetes mellitus.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fetal growth restriction (FGR) and pre-eclampsia with fetal growth restriction (PE/FGR) are high-risk perinatal diseases that may involve high levels of human chorionic gonadotropin (hCG) and mitochondrial dysfunction. However, little is known about how these factors affect placental function. We investigated how mitochondrial dysfunction and high hCG expression affected placental function in unexplained FGR and PE/FGR. We observed elevated expression of hCGβ and growth differentiation factor 15 mRNA and protein levels in the placenta with both diseases. Likewise, antiangiogenic factors, such as Ang2, IP10, sFlt1, IL8, IL1B, and TNFα, were also upregulated at the mRNA level. In addition, the expression of COXI and COXII which encoded by mitochondrial DNA were significantly decreased in both diseases, suggesting that mitochondrial translation was impaired. Treatment with hCG increased Ang2, IP10, IL8, and TNFα mRNA levels in a dose-dependent manner via the p38 and JNK pathways. Mitochondrial translation inhibitors increased hCGβ expression through stabilization of HIF1α, and increased IL8 and TNFα mRNA expression. These results revealed that high expression of hCG due to mitochondrial translational dysfunction plays an important role in the pathogenesis of FGR and PE/FGR.
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