Evidence map›Paper›PMID 32594840›Full record

ArticleCell cycle (Georgetown, Tex.)2020

BMI1 promotes steroidogenesis through maintaining redox homeostasis in mouse MLTC-1 and primary Leydig cells.

Tingting Gao, Meng Lin, Binbin Shao, Qiao Zhou, Yufeng Wang, Xia Chen, Dan Zhao, Xiuliang Dai, Cong Shen, Hongbo Cheng and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.2field-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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  4. Dcun1d3 is dispensable for spermatogenesis and male fertility in mice.American journal of clinical and experimental immunology · 2025
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  5. DCUN1D2 is insignificant for spermatogenesis and male fertility in mice.American journal of translational research · 2025
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  8. PeerJ · 2023
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  12. Long non-coding RNAThe Journal of international medical research · 2022
    Article
  13. Article
  14. Testis-enrichedTranslational andrology and urology · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. E3 ubiquitin ligase ASB17 is required for spermiation in mice.Translational andrology and urology · 2021
    Article
  20. 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

17 authors at 5 institutions in 1 country.

Tingting GaoCenter of Clinical Reproductive Medicine, The Affiliated Changzhou Matemity and Child Health Care Hospital of Nanjing Medical University , Changzhou, China.
Meng LinState Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University , Nanjing, China.
Binbin ShaoDepartment of Prenatal Diagnosis, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital , Nanjing, China.
Qiao ZhouDepartment of Reproduction, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital , Nanjing, China.
Yufeng WangCenter of Clinical Reproductive Medicine, The Affiliated Changzhou Matemity and Child Health Care Hospital of Nanjing Medical University , Changzhou, China.
Xia ChenDepartment of Obstetrics and Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University , Zhenjiang, China.
Dan ZhaoFourth Affiliated Hospital of Jiangsu University , Zhenjiang, China.
Xiuliang DaiCenter of Clinical Reproductive Medicine, The Affiliated Changzhou Matemity and Child Health Care Hospital of Nanjing Medical University , Changzhou, China.
Cong ShenCenter for Reproduction and Genetics, NHC Key Laboratory of Male Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University , Suzhou, China.ORCID 0000-0002-9982-176X
Hongbo ChengCenter for Reproduction and Genetics, NHC Key Laboratory of Male Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University , Suzhou, China.
Shenmin YangCenter for Reproduction and Genetics, NHC Key Laboratory of Male Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University , Suzhou, China.
Hong LiCenter for Reproduction and Genetics, NHC Key Laboratory of Male Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University , Suzhou, China.
Bo ZhengCenter for Reproduction and Genetics, NHC Key Laboratory of Male Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University , Suzhou, China.ORCID 0000-0002-1496-0753
Xingming ZhongNHC Key Laboratory of Male Reproduction and Genetics , Guangdong, China.
Jun YuDepartment of Obstetrics and Gynecology, Affiliated Hospital of Jiangsu University, Jiangsu University , Zhenjiang, China.
Li ChenCenter of Clinical Reproductive Medicine, The Affiliated Changzhou Matemity and Child Health Care Hospital of Nanjing Medical University , Changzhou, China.
Xiaoyan HuangState Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University , Nanjing, China.
Nanjing Maternity and Child Health Care Hospital · CNSuzhou Municipal Hospital · CNJiangsu University · CNNanjing Medical University · CNGuangdong Provincial Family Planning Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In males, aging is accompanied by decline in serum testosterone levels due to impairment of testicular Leydig cells. The polycomb protein BMI1 has recently been identified as an anti-aging factor. In our previous study, BMI1 null mice showed decreased serum testosterone and Leydig cell population, excessive oxidative stress and p16/p19 signaling activation. However, a cause-and-effect relationship between phenotypes and pathways was not investigated. Here, we used the rescue approach to study the role of oxidative stress or p16/p19 in BMI1-mediated steroidogenesis. Our results revealed that treatment with antioxidant NAC, but not down-regulation of p16/p19, largely rescued cell senescence, DNA damage and steroidogenesis in BMI1-deficient mouse MLTC-1 and primary Leydig cells. Collectively, our study demonstrates that BMI1 orchestrates steroidogenesis mainly through maintaining redox homeostasis, and thus, BMI1 may be a novel and potential therapeutic target for treatment of hypogonadism.

Indexed as

HomeostasisAcetylcysteineAnimalsAntioxidantsApoptosisCell CycleCell ProliferationCells, CulturedCell SurvivalCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p19Heterocyclic Compounds, 2-RingLeydig CellsMaleMiceModels, BiologicalAcetylcysteineAntioxidantsBmi1 protein, mouseCdkn2d protein, mouseCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p19Heterocyclic Compounds, 2-RingPolycomb Repressive Complex 1Proto-Oncogene ProteinsPTC-209Reactive Oxygen SpeciesSteroidsTestosteroneThiazolesBMI1Leydig cellsoxidative stressp16/p19 signalingsteroidogenesis

Identifiers

PMID32594840
PMCPMC7469621
OpenAlexW3037721715

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.