Evidence map›Paper›PMID 37642904›Full record

ArticleJournal of endocrinological investigation2024

Maternal androgen excess inhibits fetal cardiomyocytes proliferation through RB-mediated cell cycle arrest and induces cardiac hypertrophy in adulthood.

Y Huo, W Wang, J Zhang, D Xu, F Bai, Y Gui

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of endocrinological investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

6 authors at 4 institutions in 1 country.

Y HuoNational Children's Medical Center, Children's Hospital of Fudan University, Fudan University, Shanghai, 201102, China.
W WangGuangzhou Center for Disease Control and Prevention, Guangzhou, 510080, China.
J ZhangNational Children's Medical Center, Children's Hospital of Fudan University, Fudan University, Shanghai, 201102, China.
D XuNational Children's Medical Center, Children's Hospital of Fudan University, Fudan University, Shanghai, 201102, China.
F BaiNational Children's Medical Center, Children's Hospital of Fudan University, Fudan University, Shanghai, 201102, China.
Y GuiNational Children's Medical Center, Children's Hospital of Fudan University, Fudan University, Shanghai, 201102, China. yhgui_sh@163.com.
National Health and Family Planning Commission · CNChildren's Hospital of Fudan University · CNFudan University · CNGuangzhou Center for Disease Control and Prevention · CN

Funding

construction of Innovation Platform for Early Childhood Health and Maintenance XM06221237
6 · The paper itself

Abstract

purposeMaternal hyperandrogenism during pregnancy is associated with adverse gestational outcomes and chronic non-communicable diseases in offspring. However, few studies are reported to demonstrate the association between maternal androgen excess and cardiac health in offspring. This study aimed to explore the relation between androgen exposure in utero and cardiac health of offspring in fetal and adult period. Its underlying mechanism is also illustrated in this research.

methodsPregnant mice were injected with dihydrotestosterone (DHT) from gestational day (GD) 16.5 to GD18.5. On GD18.5, fetal heart tissue was collected for metabolite and morphological analysis. The hearts from adult offspring were also collected for morphological and qPCR analysis. H9c2 cells were treated with 75 μM androsterone. Immunofluorescence, flow cytometry, qPCR, and western blot were performed to observe cell proliferation and explore the underlying mechanism.

resultsIntrauterine exposure to excessive androgen led to thinner ventricular wall, decreased number of cardiomyocytes in fetal offspring and caused cardiac hypertrophy, compromised cardiac function in adult offspring. The analysis of steroid hormone metabolites in fetal heart tissue by ultra performance liquid chromatography and tandem mass spectrometry showed that the content of androgen metabolite androsterone was significantly increased. Mechanistically, H9c2 cells treated with androsterone led to a significant decrease in phosphorylated retinoblastoma protein (pRB) and cell cycle-related protein including cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 4 (CDK4), and cyclin D1 (CCND1) in cardiomyocytes. This resulted in cell cycle arrest at G1-S phase, which in turn inhibited cardiomyocyte proliferation.

conclusionTaken together, our results indicate that in utero exposure to DHT, its metabolite androsterone could directly decrease cardiomyocytes proliferation through cell cycle arrest, which has a life-long-lasting effect on cardiac health. Our study highlights the importance of monitoring sex hormones in women during pregnancy and the follow-up of cardiac function in offspring with high risk of intrauterine androgen exposure.

Indexed as

AndrogensMyocytes, CardiacAdultAndrosteroneAnimalsCardiomegalyCell Cycle CheckpointsCell Cycle ProteinsCell ProliferationDihydrotestosteroneFemaleHumansMicePregnancyAndrogensAndrosteroneCell Cycle ProteinsDihydrotestosteroneAndrogen excessCardiac functionCardiomyocytes’ proliferationDOHaD

Identifiers

PMID37642904
PMCPMC10904501
OpenAlexW4386253975

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.