Evidence map›Paper›PMID 31247506›Full record

ArticleRedox biology2019

Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution.

Renuga Devi Rajaram, Romain Dissard, Anna Faivre, Frédérique Ino, Vasiliki Delitsikou, Vincent Jaquet, Thomas Cagarelli, Maja Lindenmeyer, Pidder Jansen-Duerr, Clemens Cohen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024
    Review
  5. Article
  6. Article
  7. A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Evolution of hypoxia and hypoxia-inducible factor asparaginyl hydroxylase regulation in chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Cells · 2022
    Article
  14. Review
  15. Review
  16. Di-Tyrosine Crosslinking andAntioxidants (Basel, Switzerland) · 2021
    Article
  17. Review
  18. Nox4 Maintains Blood Pressure during Low Sodium Diet.Antioxidants (Basel, Switzerland) · 2021
    Article
  19. Article
  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

12 authors at 5 institutions in 3 countries.

Renuga Devi RajaramLaboratory of Nephrology, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland; Service of Nephrology, Department of Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland.
Romain DissardLaboratory of Nephrology, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland; Service of Nephrology, Department of Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland.
Anna FaivreLaboratory of Nephrology, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland; Service of Nephrology, Department of Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland.
Frédérique InoLaboratory of Nephrology, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland; Service of Nephrology, Department of Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland.
Vasiliki DelitsikouLaboratory of Nephrology, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland; Service of Nephrology, Department of Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland.
Vincent JaquetDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Thomas CagarelliService of Clinical Pathology, Department of Pathology and Immunology, University Hospital and University of Geneva, Geneva, Switzerland.
Maja LindenmeyerNephrological Center Medical Clinic and Polyclinic IV, University of Munich, Munich, Germany; III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Pidder Jansen-DuerrUniversität Innsbruck, Research Institute for Biomedical Aging Research, Rennweg 10, Innsbruck, Austria.
Clemens CohenNephrological Center Medical Clinic and Polyclinic IV, University of Munich, Munich, Germany.
Solange MollService of Clinical Pathology, Department of Pathology and Immunology, University Hospital and University of Geneva, Geneva, Switzerland.
Sophie de SeigneuxLaboratory of Nephrology, Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland; Service of Nephrology, Department of Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland. Electronic address: Sophie.deseigneux@hcuge.ch.
University of Geneva · CHUniversity Hospital of Geneva · CHLudwig-Maximilians-Universität München · DEUniversität Hamburg · DEUniversität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNADPH oxidase 4 (NOX4) catalyzes the formation of hydrogen peroxide (H

methodsWe performed immunostaining with a specific anti-NOX4 antibody and measured NOX4 mRNA expression in human renal biopsies encompassing diverse renal diseases. We generated transgenic mice specifically overexpressing mouse Nox4 in renal tubular cells and subjected the animals to the unilateral ureteral obstruction (UUO) model of fibrosis.

resultsIn normal human kidney, NOX4 protein expression was at its highest on the basolateral side of proximal tubular cells. NOX4 expression increased in mesangial cells and podocytes in proliferative diabetic nephropathy. In tubular cells, NOX4 protein expression decreased in all types of chronic renal disease studied. This finding was substantiated by decreased NOX4 mRNA expression in the tubulo-interstitial compartment in a repository of 175 human renal biopsies. Overexpression of tubular NOX4 in mice resulted in enhanced renal production of H

conclusionsNOX4 expression was decreased in tubular cells in all types of CKD tested. Tubular NOX4 overexpression did not induce injury in the kidney, and neither modified microvascularization, nor kidney structural lesions in fibrosis.

Indexed as

AnimalsBiopsyDiabetic NephropathiesDisease Models, AnimalFibrosisGene Expression RegulationGlomerular Filtration RateHumansHydrogen PeroxideKidney TubulesMaleMesangial CellsMiceMice, TransgenicNADPH Oxidase 4NF-E2-Related Factor 2Hydrogen PeroxideNADPH Oxidase 4Nfe2l2 protein, mouseNF-E2-Related Factor 2NOX4 protein, humanNox4 protein, mouseRNA, MessengerChronic kidney diseaseDiabetesIgA nephropathyKidney fibrosisNOX4Renal biopsyTubular cells

Identifiers

PMID31247506
PMCPMC6598841
OpenAlexW2948562352

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.