Evidence mapPaperPMID 36641458Full record

ArticleJournal of ovarian research2023

Androgen increases klotho expression via the androgen receptor-mediated pathway to induce GCs apoptosis.

Xin Zeng, Qiaoqing Zhong, Ming Li, Yating Liu, Shuanglian Long, Yuanjie Xie, Zhongcheng Mo

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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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

7 authors at 3 institutions in 2 countries.

Xin ZengGuangxi Key Laboratory of Diabetic Systems Medicine, Guangxi Province Postgraduate Co-Training Base for Cooperative Innovation in Basic Medicine, Guilin Medical University, Guilin, 541199, Guangxi, China.
Qiaoqing Zhong *Department of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, 410008, China.
Ming LiGuangxi Key Laboratory of Diabetic Systems Medicine, Guangxi Province Postgraduate Co-Training Base for Cooperative Innovation in Basic Medicine, Guilin Medical University, Guilin, 541199, Guangxi, China.
Yating LiuClinical Anatomy & Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Shuanglian LongClinical Anatomy & Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Yuanjie XieGuangxi Key Laboratory of Diabetic Systems Medicine, Guangxi Province Postgraduate Co-Training Base for Cooperative Innovation in Basic Medicine, Guilin Medical University, Guilin, 541199, Guangxi, China. charlesking8888@163.com.
Zhongcheng MoGuangxi Key Laboratory of Diabetic Systems Medicine, Guangxi Province Postgraduate Co-Training Base for Cooperative Innovation in Basic Medicine, Guilin Medical University, Guilin, 541199, Guangxi, China. zhchmo@hotmail.com.
Guilin Medical University · CNUniversity of South China · CNBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMany epidemiological studies have shown that anovulatory polycystic ovary syndrome (PCOS) is accompanied by hyperandrogenism. However, the exact mechanism of hyperandrogen-induced anovulation remains to be elucidated. In this study, we aimed to investigate the potential mechanism of anovulation in PCOS. To investigate the role of klotho as a key factor in the androgen receptor (AR)-mediated development of PCOS, we investigated the effects of testosterone on ovarian klotho expression in vivo and in vitro.

resultsTestosterone propionate (TP)-induced rats showed cycle irregularity, hyperandrogenism, polycystic ovarian changes, dyslipidemia. However, inhibition of AR expression could relieve PCOS traits. We also found that AR and klotho showed relatively high expression in PCOS rat ovarian tissue and in TP-induced granulosa cells (GCs), which was inhibited by the addition of flutamide. TP-induced GCs apoptosis was suppressed by AR antagonist, as well as silencing klotho expression in human GCs. Chromatin immunoprecipitation assay demonstrated that AR indirectly binds to the klotho promoter.

conclusionsOur results demonstrated TP mediates the expression of klotho via androgen receptor and klotho alterations could be a reason for ovarian dysfunction in PCOS.

Indexed as

AndrogensAnovulationHyperandrogenismKlotho ProteinsPolycystic Ovary SyndromeAnimalsApoptosisFemaleGranulosa CellsHumansRatsReceptors, AndrogenAndrogensKlotho ProteinsReceptors, AndrogenAndrogen receptorKlothoPolycystic ovarian syndromeTestosterone propionate

Identifiers

PMID36641458
PMCPMC9840339
OpenAlexW4316096808

What Socratic holds

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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 Socratic graph.