Evidence map›Paper›PMID 31924670›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Injured Podocytes Are Sensitized to Angiotensin II-Induced Calcium Signaling.

Julia Binz-Lotter, Christian Jüngst, Markus M Rinschen, Sybille Koehler, Peter Zentis, Astrid Schauss, Bernhard Schermer, Thomas Benzing, Matthias J Hackl

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. The CaPediatric nephrology (Berlin, Germany) · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Renin-angiotensin system-mediated nitric oxide signaling in podocytes.American journal of physiology. Renal physiology · 2024
    Article
  10. Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

9 authors.

Julia Binz-LotterDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; and.ORCID 0000-0003-4678-0703
Christian JüngstCologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Cologne, Germany.ORCID 0000-0002-6586-7129
Markus M RinschenDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; and.
Sybille KoehlerDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; and.
Peter ZentisCologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Cologne, Germany.ORCID 0000-0002-6999-132X
Astrid SchaussCologne Excellence Cluster on Cellular Stress Response in Aging-Associated Diseases, University of Cologne, Cologne, Germany.
Bernhard SchermerDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; and.
Thomas BenzingDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; and.
Matthias J HacklDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany; and matthias.hackl@uk-koeln.de.ORCID 0000-0002-4199-3374

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInhibition of angiotensin II (AngII) signaling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through regulating glomerular blood flow and reducing filtration pressure. Although extravascular actions of AngII have been suggested, a direct effect of AngII on podocytes has not been demonstrated

methodsTo study the effects of AngII on podocyte calcium levels

resultsIn healthy animals, podocytes displayed limited responsiveness to AngII stimulation. In contrast, in animals subjected to either adriamycin-induced acute chemical injury or genetic deletion of the podocin-encoding gene

conclusionsOur discovery that podocytes become sensitized to AngII-induced calcium signaling upon injury might explain results from large, randomized, controlled trials in which improved renal outcomes occur only in the subgroup of patients with proteinuria, indicating podocyte damage. Our findings also emphasize the need to treat every patient with a glomerular disease with either an angiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor blocker.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsCalcium SignalingCells, CulturedDisease Models, AnimalGlomerulonephritisHumansIntracellular Signaling Peptides and ProteinsKidney GlomerulusLosartanMaleMembrane ProteinsMicePodocytesProteinuriaRandom AllocationAngiotensin-Converting Enzyme InhibitorsIntracellular Signaling Peptides and ProteinsLosartanMembrane ProteinsNPHS2 proteinReceptor, Angiotensin, Type 1AASK (African American Study of Kidney Disease and Hypertension)angiotensincalciumglomerular diseasenephrinpodocyte

Identifiers

PMID31924670
PMCPMC7062224

What OpenQuestion holds

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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.