ArticleClinical epigenetics2025
Folic acid ameliorates placental structure and function in fetal growth restriction via epigenetic modifications.
Article in Clinical epigenetics, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Choline and Its Companions: Inter-Related Roles of Choline and B Vitamins in Fetal Development and Offspring Health.Nutrients · 2026Review
- The gut microbiota-metabolite-target axis in insomnia: network pharmacology and gut microbiota profiling insights into pathogenesis and intervention with Cinnamomi Cortex-Gardeniae Fructus.Frontiers in microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundFetal growth restriction (FGR) is associated with perinatal complications and potential neurodevelopmental risks, yet mechanistic understanding of metabolic dysregulation remains incomplete. We investigated amniotic fluid metabolites as potential functional biomarkers of fetal-placental dysfunction and explored the possibility of folic acid-mediated epigenetic remediation of metabolic imbalances in FGR.
resultsIn FGR amniotic fluid, hypoxanthine was significantly upregulated, valproic acid (VPA) was significantly downregulated, and arginine/proline metabolism pathways were markedly enriched. Folic acid intervention significantly improved fetal growth parameters (crown-rump length, body weight, and placental weight; all P < 0.001). Compensatory labyrinth zone (Lb) hyperplasia was observed in FGR placenta, with a 40% increase in Lb/Jz ratio, while folic acid supplementation reduced Lb proportion by 10% and appeared to restore placental architecture. Epigenetically, folic acid supplementation suppressed histone deacetylases1 (HDAC1) expression, elevated H3K9ac levels and enhanced trophoblast proliferation.
conclusionsOur research suggests that dysregulation of the VPA-hypoxanthine axis may serve as a hallmark of FGR-associated metabolic stress. Folic acid may exerts potential dual therapeutic effects by correcting placental architecture through Lb normalization and initiating epigenetic reprogramming via HDAC1 inhibition and acetylation at lysine 9 of histone H3 (H3K9ac). These findings indicate that folate metabolism could play a regulatory role in placental gene transcription and fetal growth trajectories.
Indexed as
Identifiers
What Socratic holds
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.