Evidence map›Paper›PMID 39981520›Full record

ArticleiScience2025

17β-estradiol and estrogen receptor alpha protect mouse ovarian follicle development by repressing atresia.

Eri Ueno, Mitsuya Watanabe, Yoshiko Kondo, Naomi Nakagata, Toru Takeo, Satohiro Nakao, Katsueki Ogiwara

Abstract read
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Protective effects ofFrontiers in pharmacology · 2025
    Article
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

7 authors.

Eri UenoLaboratory of Reproductive and Developmental Biology, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.
Mitsuya WatanabeLaboratory of Reproductive and Developmental Biology, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.
Yoshiko KondoLaboratory of Reproductive and Developmental Biology, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.
Naomi NakagataDivision of Reproductive Biotechnology and Innovation, Center for Animal Resources and Development, Institute of Resource Development and Analysis, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan.
Toru TakeoDivision of Reproductive Engineering, Center for Animal Resources and Development, Institute of Resource Development and Analysis, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan.
Satohiro NakaoDivision of Reproductive Engineering, Center for Animal Resources and Development, Institute of Resource Development and Analysis, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan.
Katsueki OgiwaraLaboratory of Reproductive and Developmental Biology, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice administered an inhibin antiserum, equine chorionic gonadotropin (eCG) mixture called CARD HyperOva (OVA)/human chorionic gonadotropin (hCG), ovulate more oocytes than those administered eCG/hCG. In this study, the mechanism by which more oocytes are ovulated was investigated. Apoptotic cells were not observed in ovaries 24 and 48 h after OVA injection, and INHBA expression was absent in the growing follicles with apoptotic cells, whereas granulosa cells in follicles expressing INHBA also expressed estrogen receptor α (ESR1). ESR1 and CYP19A1 expression and 17β-estradiol (E

Indexed as

EndocrinologyMolecular physiologyRodent reproduction

Identifiers

PMID39981520
PMCPMC11841210

What OpenQuestion 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 OpenQuestion graph.