Evidence map›Paper›PMID 23130103›Full record

ArticlePulmonary circulation2012

Testosterone negatively regulates right ventricular load stress responses in mice.

Anna R Hemnes, Karen B Maynard, Hunter C Champion, Linda Gleaves, Niki Penner, James West, John H Newman

Open access · bronzeAbstract read
In one paragraph

Article in Pulmonary circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
  2. Article
  3. Women's heart and echocardiography.Journal of cardiovascular imaging · 2026
    Review
  4. Right Heart Diastology, Where Are We Now?Circulation research · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Investigating the "sex paradox" in pulmonary arterial hypertension: Results from the Pulmonary Hypertension Association Registry (PHAR).The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2024
    Article
  10. Review
  11. Review
  12. Y-Chromosome Gene,American journal of respiratory and critical care medicine · 2022
    Article
  13. Review
  14. Sex and gender in pulmonary arterial hypertension.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  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

7 authors at 2 institutions in 1 country.

Anna R HemnesDivision of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Karen B Maynard
Hunter C Champion
Linda Gleaves
Niki Penner
James West
John H Newman
Vanderbilt University Medical Center · USUniversity of Pittsburgh Medical Center · US

Funding

Interventions Against the Molecular Etiology of BMPR2-induced PAHR01HL095797 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WEST, JAMES D · 2010 to 2022
$6.7M
Gender differences and endothelin responses in right ventricular afterload stressK08HL093363 · NHLBI · VANDERBILT UNIVERSITY · PI HEMNES, ANNA R · 2008 to 2012
$627k
NHLBI NIH HHS K08 HL093363NHLBI NIH HHS R01 HL095797
6 · The paper itself

Abstract

Right ventricular (RV) function is the major determinant of mortality in pulmonary arterial hypertension and male sex is a strong predictor of mortality in this disease. The effects of testosterone on RV structure and function in load stress are presently unknown. We tested whether testosterone levels affect RV hypertrophic responses, fibrosis, and function. Male C57BL/6 mice underwent castration or sham followed by pulmonary artery banding (PAB) or sham. After recovery, testosterone pellets were placed in a subset of the castrated mice and mice were maintained for at least two weeks, when they underwent hemodynamic measurements and tissues were harvested. Plasma levels of testosterone were reduced by castration and repleted by testosterone administration. In PAB, castration resulted in lower right ventricle/left ventricle + septum (RV/LV+S), and myocyte diameter (P < 0.05). Replacement of testosterone normalized these parameters and increased RV fibrosis (P < 0.05). Two weeks of PAB resulted in increased RV systolic pressure in all groups with decreased markers of RV systolic and diastolic function, specifically reduced ejection fraction and increased time constant, and dPdt minimum (P < 0.05), though there was minimal effect of testosterone on hemodynamic parameters. Survival was improved in mice that underwent castration with PAB compared with PAB alone (P < 0.05). Testosterone affects RV hypertrophic response to load stress through increased myocyte size and increased fibrosis in mice. Castration and testosterone replacement are not accompanied by significant alterations in RV in vivo hemodynamics, but testosterone deprivation appears to improve survival in PAB. Further study of the role of testosterone in RV dysfunction is warranted to better understand these findings in the context of human disease.

Indexed as

pulmonary hypertensionright ventriclesex hormonestestosterone

Identifiers

PMID23130103
PMCPMC3487303
OpenAlexW1970248508

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.