Evidence map›Paper›PMID 20962747›Full record

ArticleKidney international2011

Testosterone and 17β-estradiol have opposite effects on podocyte apoptosis that precedes glomerulosclerosis in female estrogen receptor knockout mice.

Sophie Doublier, Enrico Lupia, Paola Catanuto, Simone Periera-Simon, Xiaomei Xia, Ken Korach, Mariana Berho, Sharon J Elliot, Michael Karl

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 8% 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

76 citing papers in PubMed, 2 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Renal Tubule Cell-SpecificHypertension (Dallas, Tex. : 1979) · 2026
    Article
  5. Review
  6. Article
  7. Kidney Health and Gender-Affirming Hormone Therapy for Transgender and Gender Diverse Individuals.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Podocyte cell-specificPhysiological genomics · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Sophie DoublierStudy Group and Laboratory on Sex and Gender Differences in Health and Disease, Department of Surgery, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA.
Enrico Lupia
Paola Catanuto
Simone Periera-Simon
Xiaomei Xia
Ken Korach
Mariana Berho
Sharon J Elliot
Michael Karl
University of Miami · USNational Institutes of Health · USHodges University · US

Funding

Chemical Receptor Interactions In Reproduction And Hormonal ToxicityZIAES070065 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KORACH, KENNETH S · 2009 to 2019
$29.6M
ESTROGEN DEFICIENCY AND RENAL DISEASE IN AGING WOMENR01AG017170 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ELLIOT, SHARON J · 1999 to 2012
$4.6M
Intramural NIH HHS ZIA ES070065NIA NIH HHS R01 AG017170NIA NIH HHS R01AG17170-06
6 · The paper itself

Abstract

Podocyte damage and apoptosis are thought to be important if not essential in the development of glomerulosclerosis. Female estrogen receptor knockout mice develop glomerulosclerosis at 9 months of age due to excessive ovarian testosterone production and secretion. Here, we studied the pathogenesis of glomerulosclerosis in this mouse model to determine whether testosterone and/or 17β-estradiol directly affect the function and survival of podocytes. Glomerulosclerosis in these mice was associated with the expression of desmin and the loss of nephrin, markers of podocyte damage and apoptosis. Ovariectomy preserved the function and survival of podocytes by eliminating the source of endogenous testosterone production. In contrast, testosterone supplementation induced podocyte apoptosis in ovariectomized wild-type mice. Importantly, podocytes express functional androgen and estrogen receptors, which, upon stimulation by their respective ligands, have opposing effects. Testosterone induced podocyte apoptosis in vitro by androgen receptor activation, but independent of the TGF-β1 signaling pathway. Pretreatment with 17β-estradiol prevented testosterone-induced podocyte apoptosis, an estrogen receptor-dependent effect mediated by activation of the ERK signaling pathway, and protected podocytes from TGF-β1- or TNF-α-induced apoptosis. Thus, podocytes are target cells for testosterone and 17β-estradiol. These hormones modulate podocyte damage and apoptosis.

Indexed as

AnimalsApoptosisCell DedifferentiationDesminEstradiolEstrogen Receptor alphaEstrogen Receptor betaFemaleGene ExpressionGlomerulosclerosis, Focal SegmentalIn Vitro TechniquesMembrane ProteinsMiceMice, KnockoutOvariectomyPodocytesDesminEstradiolEstrogen Receptor alphaEstrogen Receptor betaMembrane ProteinsnephrinReceptors, AndrogenSmad7 ProteinSmad7 protein, mouseTestosteroneTransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID20962747
PMCPMC4775100
OpenAlexW1990060718

What OpenQuestion holds

Textmetadata
LicenceTDM
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.