Evidence map›Paper›PMID 39453929›Full record

ArticlePloS one2024

The mechanism of NF-κB-TERT feedback regulation of granulosa cell apoptosis in PCOS rats.

Haoxuan Xue, Zecheng Hu, Shun Liu, Shun Zhang, Wenqin Yang, Jiasi Li, Chulin Yan, Jiaming Zhang, Jing Zhang, Xiaocan Lei

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  5. Article
  6. Mice lacking NF-ĸB1 undergo premature ovarian aging.Reproductive biology and endocrinology : RB&E · 2026
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  17. Natural solutions for glowing skin: spices.Frontiers in nutrition · 2025
    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

10 authors.

Haoxuan XueThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Zecheng HuDepartment of Breast and Thyroid Surgery, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Shun LiuThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Shun ZhangDepartment of Reproductive Medical Center, The Affiliated Hospital of Guilin Medical University, Guilin, China.
Wenqin YangThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Jiasi LiThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Chulin YanThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Jiaming ZhangThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.ORCID 0009-0003-2309-5882
Jing ZhangThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Xiaocan LeiThe First Affiliated Hospital, Gynecology & Obstetrics and Reproductive Medical Center, Clinical Anatomy and Reproductive Medicine Application Institute, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with Polycystic ovary syndrome (PCOS) have chronic low-grade ovarian inflammation. Inflammation can cause telomere dysfunction, and telomere and telomerase complex are also involved in regulating inflammation. However, the specific mechanisms of inflammatory signaling feedback and telomere-telomerase mutual regulation remain to be discovered. This study elucidates the role of Nuclear factor kappa-B (NF-κB)-Telomerase reverse transcriptase (TERT) feedback in PCOS granulosa cell apoptosis. Using letrozole and a high-fat diet, a PCOS rat model was established, along with a Lipopolysaccharide (LPS) -treated KGN cell inflammation model was established. NF-κB and TERT inhibitors (BAY 11-7082 and BIBR1532) were then administered to LPS-induced KGN cells. PCOS rats displayed disrupted estrous cycles, increased weight, elevated serum testosterone, cystic follicles, granulosa cell layer thinning, and reduced corpora lutea count (P are all less than 0.05). In PCOS rat ovaries, NF-κB, Interleukin-6 (IL-6), Tumor Necrosis Factor α (TNF-α), TERT, Bax, and Caspase-3 exhibited notable upregulation, while Bcl-2 decreased, with telomere elongation (P are all less than 0.05). There were significant correlations among NF-κB-related inflammatory factors, TERT and apoptotic factors, and they were positively correlated with Bax and Caspase-3, and negatively correlated with Bcl-2 (P are all less than 0.05). LPS-treated KGN cells demonstrated increased expression of inflammatory and pro-apoptotic factors, later restored post-treatment with NF-κB and TERT inhibitors (P are all less than 0.05). In conclusion, TERT may induce granulosa cell apoptosis by participating in the regulation of the NF-κB signaling pathway, thereby mediating the chronic inflammatory response of PCOS through downstream inflammatory factors IL-6 and TNF-α.

Indexed as

ApoptosisGranulosa CellsPolycystic Ovary SyndromeTelomeraseAnimalsDisease Models, AnimalFeedback, PhysiologicalFemaleHumansInflammationLipopolysaccharidesNF-kappa BRatsRats, Sprague-DawleySignal TransductionLipopolysaccharidesNF-kappa BTelomerase

Identifiers

PMID39453929
PMCPMC11508119

What OpenQuestion holds

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LicenceCC BY
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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.