ArticleScientific reports2021
Oxidative stress-induced impairment of trophoblast function causes preeclampsia through the unfolded protein response pathway.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Crosstalk between microRNA and Oxidative Stress in Heart Failure: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- ESRRG downregulation in early spontaneous abortion induces mitochondrial damage, leading to impaired trophoblast function.Annals of medicine · 2026Article
- CD36: bridging metabolism, inflammation, and reproduction.npj metabolic health and disease · 2026Review
- Regulation of trophoblast fusion dysfunction in preeclampsia by the NCK1/EIF3D/PPARG axis.Biological research · 2026Article
- Asperosaponin VI Ameliorates Spontaneous Abortion by Inhibiting Trophoblast Ferroptosis via the KEAP1/NRF2/GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Advantages, limitations, and innovative considerations for established and emerging models of human placental syncytiotrophoblast.Human reproduction update · 2026Review
- Dietary Glucose Oxidase Supplementation During Gestation Improves Health Status by Affecting Antioxidant Capacity, Immune Function, and Gut Microbiota of Farrowing Sows.Microorganisms · 2026Article
- Ferroptosis-related gene BACH1 is associated with preeclampsia and shows potential as a biomarker.BMC pregnancy and childbirth · 2026Article
- Aberrant Uteroplacental and Vascular Signaling and Remodeling by Matrix Metalloproteinases in Pregnancy-Related Hypertension and Preeclampsia.Biomolecules · 2026Review
- Trimester-specific reference intervals for serum N-acetyl-β-D-glucosaminidase in healthy pregnant women in Hainan, China.European journal of obstetrics & gynecology and reproductive biology: X · 2026Article
- Linking Oxidative Stress to Placental Dysfunction: The Key Role of Mitochondria in Trophoblast Function.Medical sciences (Basel, Switzerland) · 2026Review
- Integrated bioinformatics and machine learning to explore the common mechanisms and potential biomarkers between periodontitis and preterm birth.Frontiers in cell and developmental biology · 2026Article
- Hydrogen sulfide modulates gene networks in hypoxia/reoxygenation-stressed trophoblasts: insights from transcriptome profiling.Frontiers in bioinformatics · 2026Article
- Article
- The role of miRNA-17-3p, oxidative stress, and trace elements in the pathogenesis of preeclampsia.Molecular biology reports · 2025Article
- Pre-eclampsia-related TLR2/4 signaling activates NOX2/4 to induce oxidative stress and ferroptosis in trophoblasts.European journal of medical research · 2025Article
- Trophoblast Function in Preeclampsia: Decoding the Mechanistic Roles of Coding and Non-Coding Genes.International journal of molecular sciences · 2025Review
- Navigating Cellular Stress: Endoplasmic Reticulum Stress and the Unfolded Protein Response in the Molecular Pathogenesis of Preeclampsia.Cell biochemistry and biophysics · 2025Review
- Variations in blood levels of the anti-fusogenic endogenous retroviral protein suppressyn are associated with fetal growth outcome in preeclampsia.Scientific reports · 2025Article
- Localization and quantification of placentalPhysiological genomics · 2025Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pre-eclampsia (PE) is a pregnancy-specific disorder, characterized by hypertension and proteinuria. In PE, trophoblasts mediated inadequate remodeling of uterine spiral arteries seem to interrupt uteroplacental blood flow, one of the hallmarks in the early onset of PE (EO-PE). This, in turn, results in placental ischemia-reperfusion injury during hypoxia and reoxygenation episodes, leading to the generation of reactive oxygen species (ROS) and oxidative stress (OS). But still it is debatable if OS is a cause or consequence of PE. In this present study, we have investigated the effects of OS on PE placentae and trophoblast cell functions using BeWo and HTR8/SVneo cell lines. PE placental tissues showed abnormal ultrastructure, high level of reactive oxygen species (ROS) with altered unfolded protein responses (UPR) in compare with term placental tissues. Similar to PE placentae, during OS induction, the trophoblast cells showed altered invasion and migration properties with significantly variable expression of differentiation and invasion markers, e.g., syncytin and MMPs. The effect was rescued by antioxidant, N-acetyl cysteine, thereby implying a ROS-specific effect and in the trophoblast cells, OS triggers UPR pathway through IRE1α-XBP1 axis. Taken together, these findings highlight the harmful effect of unfolded protein response, which was induced due to OS on trophoblast cells and deformed invasion and differentiation programme and can be extended further to clinical settings to identify clinically approved antioxidants during pregnancy as a therapeutic measure to reduce the onset of PE.
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