Evidence map›Paper›PMID 22669940›Full record

ArticleThe Journal of biological chemistry2012

Involvement of the up-regulated FoxO1 expression in follicular granulosa cell apoptosis induced by oxidative stress.

Ming Shen, Fei Lin, Jiaqing Zhang, Yiting Tang, Wei-Kang Chen, Honglin Liu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
2.6field-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

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 187 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  16. Long Noncoding RNA NONHSAT233728.1 Promotes ROS Accumulation and Granulosa Cell Apoptosis by Regulating the MAPK/ERK1/2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  17. Article
  18. Article
  19. Observational
  20. Review

39 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Ming ShenCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
Fei Lin
Jiaqing Zhang
Yiting Tang
Wei-Kang Chen
Honglin Liu
Nanjing Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follicular atresia is common in female mammalian ovaries, where most follicles undergo degeneration at any stage of growth and development. Oxidative stress gives rise to triggering granulosa cell apoptosis, which has been suggested as a major cause of follicular atresia. However, the underlying mechanism by which the oxidative stress induces follicular atresia remains unclear. FoxO transcription factors are known as critical mediators in the regulation of oxidative stress and apoptosis. In this study, the involvement of FoxO1 in oxidative stress-induced apoptosis of mouse follicular granulosa cells (MGCs) was investigated in vivo and in vitro. It was observed that increased apoptotic signals correlated with elevated expression of FoxO1 in MGCs when mice were treated with the oxidant. Correspondingly, the expressions of FoxO1 target genes, such as proapoptotic genes and antioxidative genes, were also up-regulated. In primary cultured MGCs, treatment with H(2)O(2) led to FoxO1 nuclear translocation. Further studies with overexpression and knockdown of FoxO1 demonstrated the critical role of FoxO1 in the induction of MGC apoptosis by oxidative stress. Finally, inactivation of FoxO1 by insulin treatment confirmed that FoxO1 induced by oxidative stress played a pivotal role in up-regulating the expression of downstream apoptosis-related genes in MGCs. Our results suggest that up-regulation of FoxO1 by oxidative stress leads to apoptosis of granulosa cells, which eventually results in follicular atresia in mice.

Indexed as

ApoptosisOxidative StressUp-RegulationActive Transport, Cell NucleusAnimalsApoptosis Regulatory ProteinsCell NucleusCells, CulturedFemaleFollicular AtresiaForkhead Box Protein O1Forkhead Transcription FactorsGene Knockdown TechniquesGranulosa CellsInsulinMice3-nitropropionic acidApoptosis Regulatory ProteinsForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseInsulinNitro CompoundsOxidantsPropionatesReactive Oxygen Species

Identifiers

PMID22669940
PMCPMC3406661
OpenAlexW2070143210

What OpenQuestion holds

Textmetadata
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.