ArticleFrontiers in endocrinology2025
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Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Moderate NEFA reprogram early follicular development and oocyte competence: evidence for a targetable redox mechanism.Frontiers in nutrition · 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Assisted reproductive technologies (ART) are constrained by the limited pool of medium antral follicles. Early antral follicles (EAfs) are an emerging additional source coming either from cryopreserved ovaries or from Results: Transcriptome analysis of 22-141 genes revealed 1-386 DEGs in CCs supporting metaphase-II (MII) oocytes and 1-420 in CCs enclosing germinal-vesicle (GV) oocytes. Network modelling pinpointed as signature of competent CCs three down-regulated outliers (EFHD1, HS6ST2, SLC35G1) and two hubs (CDC6, KIF11), while the unsuccessful ones revealed six outliers (HBA1, SLC39A8, ERO1A, TKDP5, CALCRL, ELOVL6) and the hub CASP3. The profile of EAfs enclosing competent oocyte converged towards cumulus expansion and controlled cell-cycle quiescence pathways whereas lipid dysregulation, oxidative stress and apoptosis characterized CC surrounding incompetent oocytes. The endpoint comparison yielded 11 markers, highlighted by SEMA3A up-regulation and IL1A, DDIT4 and VNN1 down-regulation. qPCR confirmed the transcriptome profile of the key genes (HS6ST2, CDC6, ERO1, CASP3 and SEMA3A) while immuno-assays corroborated the differential expression and localization of some related codified driver proteins (HAS2, CASP3 and SEMA3A). Conclusions: CC transcriptomics defines a concise 12-gene driver panel plus 11 endpoint markers that accurately predict the maturation fate of individual EAfs by providing actionable targets and a practical basis for rapid, non-invasive selection of high-quality follicles, with potential to enhance fertility preservation, livestock breeding and clinical ART outcomes. In addition, the analysis point on new gene/protein mediating CCs maturation mechanism is to be considered.
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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.