Evidence map›Paper›PMID 41151533›Full record

ArticleReproduction (Cambridge, England)2025

FGF receptor 2 signaling in granulosa cells is required for normal female fertility in mice.

Takuya Kanke, Ayaka Ichikawa, Yuki Akimoto, Shunichi Matsunaga, Wataru Fujii, Tsutomu Endo, Kunihiko Naito, Koji Sugiura

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Reproduction (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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

8 authors.

Takuya KankeDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Ayaka IchikawaDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Yuki AkimotoDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Shunichi MatsunagaDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Wataru FujiiDepartment of Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Tsutomu EndoDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Kunihiko NaitoDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Koji SugiuraDepartment of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-8945-3353

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In brief: Fibroblast growth factor (FGF) signaling has been implicated in ovarian follicular development in mammals, but its in vivo role in female fertility remains unclear. This study reveals the requirement of fibroblast growth factor receptor 2 (FGFR2) signaling in ovarian granulosa cells for normal female fertility in mice, likely by regulating glycolysis in cumulus cells and enhancing oocyte developmental competence. Abstract: FGF signaling has been implicated in ovarian follicular development in mammals, but its in vivo role in female fertility remains unclear. To investigate this role, we generated granulosa cell-specific conditional knockout (cKO) mice lacking FGF receptor 2 (FGFR2). Fgfr2 cKO female mice exhibited significantly reduced fertility despite normal follicular development, estrous cycles, and ovulation. In contrast, cumulus cells in cKO mice showed decreased expression of glycolytic enzymes such as PFKP and LDHA, potentially impairing metabolic support for oocytes. Consequently, cKO cumulus cells were less competent than control cells in supporting the meiotic resumption of oocytes under in vitro conditions. Furthermore, while cKO oocytes developed into blastocysts at normal rates in vitro, their ability to reach term after embryo transfer was significantly diminished. These findings demonstrate that FGFR2-mediated FGF signaling in granulosa cells is essential for normal female fertility, likely by regulating glycolysis in cumulus cells and promoting oocyte developmental competence.

Indexed as

FertilityGranulosa CellsOocytesReceptor, Fibroblast Growth Factor, Type 2Signal TransductionAnimalsCumulus CellsFemaleGlycolysisMiceMice, KnockoutOvarian FollicleFgfr2 protein, mouseReceptor, Fibroblast Growth Factor, Type 2fibroblast growth factorglycolysisgranulosa cellsovary

Identifiers

PMID41151533
PMCPMC12574604

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.