Evidence map›Paper›PMID 27436181›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Age-associated up-regulation of EGR1 promotes granulosa cell apoptosis during follicle atresia in mice through the NF-κB pathway.

Suzhen Yuan, Jingyi Wen, Jing Cheng, Wei Shen, Su Zhou, Wei Yan, Lu Shen, Aiyue Luo, Shixuan Wang

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
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

34 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  4. The roles of RNA-binding proteins in ovarian aging.Journal of assisted reproduction and genetics · 2026
    Review
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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

9 authors at 2 institutions in 1 country.

Suzhen Yuana Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Jingyi Wena Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Jing Chenga Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Wei Shena Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Su Zhoua Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Wei Yana Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Lu Shena Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Aiyue Luoa Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Shixuan Wanga Department of Obstetrics and Gynecology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follicular atresia is the main process responsible for the loss of follicles and oocytes from the ovary, and it is the root cause of ovarian aging. Apoptosis of granulosa cells (GCs) is the cellular mechanism responsible for follicular atresia in mammals. Recent advances have highlighted fundamental roles for EGR1 in age-related diseases via the induction of apoptosis. In the present study, we found that the expression of EGR1 was significantly increased in aged mouse ovaries compared with young ovaries. Immunohistochemical analysis revealed strongly positive EGR1 staining in atretic follicles, especially in apoptotic granulosa cells. We further showed that EGR1 up-regulation in mouse primary granulosa cells inhibited cell proliferation and promoted apoptosis. In addition, the promotion of apoptosis in GCs by EGR1 increases over time and with reactive oxygen species (ROS) stimulation. Our mechanistic study suggested that EGR1 regulates GC apoptosis in a mitochondria-dependent manner and that this mainly occurs through the NF-κB signaling pathway. In conclusion, our results suggested that age-related up-regulation of EGR1 promotes GC apoptosis in follicle atresia during ovarian aging.

Indexed as

Signal TransductionAgingAnimalsApoptosisCell ProliferationEarly Growth Response Protein 1FemaleFollicular AtresiaGene Expression Regulation, DevelopmentalGranulosa CellsMice, Inbred C57BLMitochondriaNF-kappa BPTEN PhosphohydrolaseTumor Suppressor Protein p53Up-RegulationEarly Growth Response Protein 1Egr1 protein, mouseNF-kappa BPTEN PhosphohydrolaseTumor Suppressor Protein p53apoptosisEGR1follicular atresiagranulosa cellNF-κBovarian aging

Identifiers

PMID27436181
PMCPMC5105915
OpenAlexW2476000717

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.