Evidence map›Paper›PMID 28852159›Full record

ArticleScientific reports2017

Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury.

Han Zhou, Xuefei Tian, Alda Tufro, Gilbert Moeckel, Shuta Ishibe, Julie Goodwin

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. A Small Molecule Agonist of Krüppel-Like Factor 15 in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2024
    Article
  2. Protecting Podocytes in Glomerular Diseases Beyond Glucocorticoids.Journal of the American Society of Nephrology : JASN · 2024
    Article
  3. Review
  4. Inhibition of the glucocorticoid receptor attenuates proteinuric kidney diseases in multiple species.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Role of the glucocorticoid receptor in glomerular disease.American journal of physiology. Renal physiology · 2019
    Review
  17. 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 1 institution in 1 country.

Han ZhouDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, 06520, USA.
Xuefei TianDepartment of Internal Medicine, Yale University School of Medicine, New Haven, CT, 06520, USA.
Alda TufroDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, 06520, USA.
Gilbert MoeckelDepartment of Pathology, Yale University School of Medicine, New Haven, CT, 06520, USA.
Shuta IshibeDepartment of Internal Medicine, Yale University School of Medicine, New Haven, CT, 06520, USA.
Julie GoodwinDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, 06520, USA. Julie.Goodwin@yale.edu.
Yale University · US

Funding

Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2008 to 2022
$16.8M
Role of Focal Adhesion Kinase (FAK) in Nephrosis and NephritisR01DK083294 · NIDDK · YALE UNIVERSITY · PI ISHIBE, SHUTA · 2010 to 2025
$5.4M
The Role of Endocytosis and Actin Regulation in PodocytesR01DK093629 · NIDDK · YALE UNIVERSITY · PI Shuta Ishibe · 2012 to 2026
$5.1M
Endothelial glucocorticoid receptor suppresses vascular inflammationR01HL131952 · NHLBI · YALE UNIVERSITY · PI GOODWIN, JULIE · 2016 to 2025
$4.9M
Molecular characterization of a novel cause of human FSGSR01DK109434 · NIDDK · YALE UNIVERSITY · PI TUFRO, ALDA · 2017 to 2020
$2.0M
NHLBI NIH HHS L40 HL093775NHLBI NIH HHS R01 HL131952NIDDK NIH HHS P30 DK079310NIDDK NIH HHS R01 DK083294NIDDK NIH HHS R01 DK093629NIDDK NIH HHS R01 DK109434
6 · The paper itself

Abstract

Nephrotic syndrome is a common disorder in adults and children whose etiology is largely unknown. Glucocorticoids remain the mainstay of therapy in most cases, though their mechanism of action remains poorly understood. Emerging evidence suggests that immunomodulatory therapies used in nephrotic syndrome directly target the podocytes. To study how steroids directly affect the podocytes in the treatment of proteinuria, we created a mouse model with podocyte-specific deletion of the glucocorticoid receptor. The podocyte-specific glucocorticoid receptor (GR) knockout mice had similar renal function and protein excretion compared to wild type. However, after glomerular injury induced by either LPS or nephrotoxic serum, the podocyte GR knockout mice demonstrated worsened proteinuria compared to wild type. Ultrastructural examination of podocytes confirmed more robust foot process effacement in the knockout animals. Expression of several key slit diaphragm protein was down regulated in pGR KO mice. Primary podocytes isolated from wild type and podocyte GR knockout mice showed similar actin stress fiber staining patterns in unstimulated conditions. Yet, when exposed to LPS, GR knockout podocytes demonstrated fewer stress fibers and impaired migration compared to wild type podocytes. We conclude that the podocyte glucocorticoid receptor is important for limiting proteinuria in settings of podocyte injury.

Indexed as

ActinsAllelesAnimalsCell MovementDisease Models, AnimalFemaleFluorescent Antibody TechniqueFocal Adhesion Kinase 1GenotypeLipopolysaccharidesMaleMiceMice, KnockoutNephrotic SyndromePodocytesProteinuriaActinsFocal Adhesion Kinase 1LipopolysaccharidesPtk2 protein, mouseReceptors, Glucocorticoid

Identifiers

PMID28852159
PMCPMC5575043
OpenAlexW2750213021

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.