Evidence map›Paper›PMID 40246835›Full record

ArticleNature communications2025

Granulosa cell transcription is similarly impacted by superovulation and aging and predicts early embryonic trajectories.

Klaudija Daugelaite, Perrine Lacour, Ivana Winkler, Marie-Luise Koch, Anja Schneider, Nina Schneider, Francesca Coraggio, Alexander Tolkachov, Xuan Phuoc Nguyen, Adriana Vilkaite and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Klaudija Daugelaite *Division of Regulatory Genomics and Cancer Evolution, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0002-9002-4406
Perrine Lacour *Faculty of Biosciences, Ruprecht-Karl-University Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-4102-2823
Ivana Winkler *Division of Molecular and Computational Prevention, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Marie-Luise KochDivision of Regulatory Genomics and Cancer Evolution, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Anja SchneiderDivision of Regulatory Genomics and Cancer Evolution, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0009-0004-9225-1145
Nina SchneiderDivision of Molecular and Computational Prevention, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Francesca CoraggioDivision of Molecular and Computational Prevention, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Alexander TolkachovDivision of Regulatory Genomics and Cancer Evolution, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Xuan Phuoc NguyenDepartment of Gynecological Endocrinology and Fertility Disorders, University Women's Hospital Heidelberg, Heidelberg, Germany.
Adriana VilkaiteDepartment of Gynecological Endocrinology and Fertility Disorders, University Women's Hospital Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-6863-2755
Julia RehnitzDepartment of Gynecological Endocrinology and Fertility Disorders, University Women's Hospital Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-4409-4697
Duncan T OdomDivision of Regulatory Genomics and Cancer Evolution, German Cancer Research Center (DKFZ), Heidelberg, Germany. d.odom@dkfz.de.ORCID http://orcid.org/0000-0001-6201-5599
Angela GoncalvesDivision of Molecular and Computational Prevention, German Cancer Research Center (DKFZ), Heidelberg, Germany. a.goncalves@dkfz.de.ORCID http://orcid.org/0000-0002-3890-7658

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) RE 3647/1-2EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 788937Helmholtz Association core fundingNationales Centrum für Tumorerkrankungen Heidelberg (National Centre for Tumor Diseases in Heidelberg) core funding
6 · The paper itself

Abstract

In vitro fertilization efficiency is limited in part because a fraction of retrieved oocytes fails to fertilize. Accurately evaluating their quality could significantly improve in vitro fertilization efficiency, which would require better understanding how their maturation may be disrupted. Here, we quantitatively investigate the interplay between superovulation and aging in mouse oocytes and their paired granulosa cells using a newly adapted experimental methodology. We test the hypothesis that superovulation disrupts oocyte maturation, revealing the key intercellular communication pathways dysregulated at the transcriptional level by forced hormonal stimulation. We further demonstrate that granulosa cell transcriptional markers can prospectively predict an associated oocyte's early developmental potential. By using naturally ovulated old mice as a non-stimulated reference, we show that aging and superovulation dysregulate similar genes and interact with each other. By comparing mice and human transcriptional responses of granulosa cells, we find that age-related dysregulation of hormonal responses and cell cycle pathways are shared, though substantial divergence exists in other pathways.

Indexed as

AgingEmbryonic DevelopmentGranulosa CellsSuperovulationTranscription, GeneticAnimalsFemaleFertilization in VitroGene Expression Regulation, DevelopmentalHumansMiceMice, Inbred C57BLOocytes

Identifiers

PMID40246835
PMCPMC12006393

What OpenQuestion holds

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Registered trials

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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.