Evidence map›Paper›PMID 29601583›Full record

ArticlePloS one2018

Chronic restraint stress induces excessive activation of primordial follicles in mice ovaries.

Minhua Xu, Junyan Sun, Qian Wang, Qiuwan Zhang, Chunsheng Wei, Dongmei Lai

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Depletion ofInternational journal of molecular sciences · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
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  9. Article
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  12. Article
  13. Article
  14. Primordial follicle activation as new treatment for primary ovarian insufficiency.Clinical and experimental reproductive medicine · 2019
    Review
  15. Necroptosis in stressed ovary.Journal of biomedical science · 2019
    Review
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

6 authors at 2 institutions in 1 country.

Minhua XuThe International Peace Maternity and Child Health Hospital, School of medicine, Shanghai Jiaotong University, Shanghai, China.
Junyan SunThe International Peace Maternity and Child Health Hospital, School of medicine, Shanghai Jiaotong University, Shanghai, China.
Qian WangThe International Peace Maternity and Child Health Hospital, School of medicine, Shanghai Jiaotong University, Shanghai, China.
Qiuwan ZhangThe International Peace Maternity and Child Health Hospital, School of medicine, Shanghai Jiaotong University, Shanghai, China.
Chunsheng WeiEye and ENT Hospital, Fudan University, Shanghai, China.
Dongmei LaiThe International Peace Maternity and Child Health Hospital, School of medicine, Shanghai Jiaotong University, Shanghai, China.ORCID 0000-0003-3810-2136
International Peace Maternity & Child Health Hospital · CNEye & ENT Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic stress is an important factor influencing people's health. It usually causes endocrinal disorders and a decline in reproduction in females. Although studies of both human and animals suggest a detrimental effect of stress on reproduction, the influence of chronic stress on the ovarian reservation and follicular development is still not clear. In this study, a chronic restraint stress (CRS) mouse model was used to investigate the effect of stress on ovarian reservation and follicular development and explore the underlying mechanism. In this study, after 8 weeks of CRS, primordial follicles were excessively activated in the ovaries of the CRS group compared with the control group. Further results showed that the activation of primordial follicles induced by CRS was involved in the increasing expression level of Kit ligand and its receptor Kit and the activation of phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/protein kinase B (Akt) pathway. The corticotropin-releasing hormone (CRH) is a neuropeptide released due to stress, which plays an important role in regulating follicle development. A high level of serum CRH was detected in the CRS mouse model, and the real-time polymerase chain reaction assay showed that the mRNA level of its main receptor CRHR1increased in the ovaries of the CRS mouse group. Moreover, 100nM CRH significantly improved the activation of primordial follicles in newborn mouse ovaries in vitro. These results demonstrated that CRS could induce immoderate activation of primordial follicles accompanied by the activation of Kit-PI3K signaling, in which CRH might be an important endocrine factor.

Indexed as

Stress, PhysiologicalAnimalsAnimals, NewbornBody WeightEstrous CycleFemaleMiceMice, Inbred BALB COvarian FolliclePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRestraint, PhysicalSignal TransductionTime FactorsUp-RegulationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN Phosphohydrolase

Identifiers

PMID29601583
PMCPMC5877864
OpenAlexW2794856511

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.