Evidence map›Paper›PMID 24533170›Full record

ArticlePloS one2014

High glucose induces podocyte injury via enhanced (pro)renin receptor-Wnt-β-catenin-snail signaling pathway.

Caixia Li, Helmy M Siragy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.9field-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

51 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Renal tubular (pro)renin receptor deletion exacerbates kidney injury inAmerican journal of physiology. Renal physiology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Enhanced Orai1-mediated store-operated CaThe Journal of biological chemistry · 2022
    Article
  14. Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022
    Article
  15. Article
  16. Article
  17. (Pro)renin receptor in the kidney: function and significance.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Review
  18. Review
  19. The Wnt Signaling Pathway in Diabetic Nephropathy.Frontiers in cell and developmental biology · 2021
    Review
  20. Review
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

2 authors at 1 institution in 1 country.

Caixia LiDivision of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, Virginia, United States of America.
Helmy M SiragyDivision of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, Virginia, United States of America.
University of Virginia Health System · US

Funding

Prorenin Receptors Mediate Hypertension and Kidney Disease in DiabetesR01HL091535 · NHLBI · UNIVERSITY OF VIRGINIA · PI SIRAGY, HELMY M · 2008 to 2020
$5.1M
Renin receptor provoked renal inflammationR01DK078757 · NIDDK · UNIVERSITY OF VIRGINIA · PI SIRAGY, HELMY M · 2007 to 2016
$3.3M
NHLBI NIH HHS HL091535NHLBI NIH HHS R01 HL091535NIDDK NIH HHS DK078757NIDDK NIH HHS R01 DK078757
6 · The paper itself

Abstract

(Pro)renin receptor (PRR) expression is upregulated in diabetes. We hypothesized that PRR contributes to podocyte injury via activation of Wnt-β-catenin-snail signaling pathway. Mouse podocytes were cultured in normal (5 mM) or high (25 mM) D-glucose for 3 days. Compared to normal glucose, high glucose significantly decreased mRNA and protein expressions of podocin and nephrin, and increased mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail, respectively. Confocal microscopy studies showed significant reduction in expression and reorganization of podocyte cytoskeleton protein, F-actin, in response to high glucose. Transwell functional permeability studies demonstrated significant increase in albumin flux through podocytes monolayer with high glucose. Cells treated with high glucose and PRR siRNA demonstrated significantly attenuated mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail; enhanced expressions of podocin mRNA and protein, improved expression and reorganization of F-actin, and reduced transwell albumin flux. We conclude that high glucose induces podocyte injury via PRR-Wnt-β-catenin-snail signaling pathway.

Indexed as

Animalsbeta CateninBlotting, WesternCells, CulturedFluorescent Antibody TechniqueGlucoseImmunoenzyme TechniquesMicePodocytesProrenin ReceptorReal-Time Polymerase Chain ReactionReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionSnail Family Transcription Factorsbeta CateninGlucoseProrenin ReceptorReceptors, Cell SurfaceRNA, MessengerSnail Family Transcription FactorsSweetening AgentsTranscription FactorsWnt Proteins

Identifiers

PMID24533170
PMCPMC3923071
OpenAlexW2041676345

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.