Evidence map›Paper›PMID 36662677›Full record

ArticleEndocrine connections2023

NEDD4L facilitates granulosa cell ferroptosis by promoting GPX4 ubiquitination and degradation.

Hong Tang, Xiaomei Jiang, Yu Hua, Heyue Li, Chunlan Zhu, Xiaobai Hao, Minhui Yi, Linxia Li

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Hong Tang1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Xiaomei Jiang1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Yu Hua1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Heyue Li1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Chunlan Zhu1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Xiaobai Hao1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Minhui Yi1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Linxia Li1Departments of Gynaecology and Obstetrics Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.ORCID 0000-0002-0924-6854
Shanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Polycystic ovary syndrome (PCOS) is an androgen disorder and ovarian dysfunction disease in women of reproductive age. The cell death of granulosa cells (GCs) plays an important role in the development of PCOS. However, the mechanism of GC death is still unclear. Methods: In the current study, NEDD4L was found to be elevated in PCOS GEO (Gene Expression Omnibus) databases and mouse models. The cell viability was analyzed by CCK-8 and FDA staining. The expression of ferroptosis markers was assessed by ELISA and immunofluorescence. The direct interaction of GPX4 and NEDD4L was verified by co-immunoprecipitation assay. Result: Functionally, results from CCK-8 and FDA staining demonstrated that NEDD4L inhibited the cell viability of KGN cells and NEDD4L increased the levels of iron, malonyldialdehyde, and reactive oxygen species and decreased glutathione levels. Moreover, the cell death of KGN induced by NEDD4L was blocked by ferroptosis inhibitor, suggesting that NEDD4L regulates KGN cell ferroptosis. Mechanistically, NEDD4L directly interacts with GPX4 and promotes GPX4 ubiquitination and degradation. Conclusion: Taken together, our study indicated that NEDD4L facilitates GC ferroptosis by promoting GPX4 ubiquitination and degradation and contributes to the development of PCOS.

Indexed as

ferroptosisGPX4NEDD4LPCOSubiquitination

Identifiers

PMID36662677
PMCPMC10083675
OpenAlexW4317557416

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.