ArticleiScience2024
Linking genotype to trophoblast phenotype in preeclampsia and HELLP syndrome associated with
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Understanding Preeclampsia: Integrating Placental Dysfunction, Immune Dysregulation and microRNA-Mediated Epigenetic Regulation.International journal of molecular sciences · 2026Review
- Linking Oxidative Stress to Placental Dysfunction: The Key Role of Mitochondria in Trophoblast Function.Medical sciences (Basel, Switzerland) · 2026Review
- Reduced circulating STOX1 is associated with inflammatory cytokines and insulin resistance in obese individuals: a cross-sectional study.Frontiers in nutrition · 2026Article
- Overexpression of the STOX1B isoform of STOX1 triggers preeclampsia-like symptoms through HNF4α-dependent alterations of coagulation cascades in mice.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia is a major hypertensive pregnancy disorder with a 50% heritability. The first identified gene involved in the disease is STOX1, a transcription factor, whose variant Y153H predisposes to the disease. Two rare mutations were also identified in Colombian women affected by the hemolysis, elevated liver enzyme, low platelet syndrome, a complication of preeclampsia (T188N and R364X). Here, we explore the effects of these variants in trophoblast cell models (BeWo) where STOX1 was previously invalidated. We firstly showed that STOX1 knockout alters response to oxidative stress, cell proliferation, and fusion capacity. Then, we showed that mutant versions of STOX1 trigger alterations in gene profiles, growth, fusion, and oxidative stress management. The results also reveal alterations of the STOX interaction with DNA when the mutations affected the DNA-binding domain of STOX1 (Y153H and T188N). We also reveal here that a major contributor of these effects appears to be the E2F3 transcription factor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.