ArticleiScience2025
Hypoxia in extravillous trophoblasts links maternal obesity and offspring neurobehavior.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Decoding Human Placental Cellular and Molecular Responses to Obesity and Fetal Growth.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neurodevelopmental Pathways from Maternal Obesity to Offspring Outcomes: An Umbrella Review of Cognitive and Behavioral Consequences Across Development.Healthcare (Basel, Switzerland) · 2025Review
Corrections and comments
- Update of
Authors and funding
7 authors.
Funding
Abstract
While maternal obesity (MO) is associated with neurobehavioral impairment (NBI) in offspring, the underlying mechanisms remain unknown. The placenta is thought to play a role in fetal programming. To elucidate the association between MO and offspring NBI, we performed single-nucleus RNA-seq on maternal- and fetal-facing sides of human term placentas from MO and lean groups. MO placentas showed the upregulation of hypoxia response genes in multiple cell types, and maternal-facing hypoxia gene expression correlated with offspring NBI in an independent birth cohort, Gen3G. Extravillous trophoblasts (EVTs) showed the highest expression of NBI-correlated genes, and EVT NBI-gene expression correlated with hypoxia signatures in two cohorts. Exposing cultured EVTs to hypoxia increased NBI gene expression, and 44% of the association between maternal BMI and NBI-gene expression in EVTs was mediated by hypoxia. Our findings suggest that hypoxia in EVTs is a key process in the neurodevelopmental programming of fetal exposure to MO.
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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 OpenQuestion graph.