Evidence map›Paper›PMID 28064162›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2017

Acute genetic ablation of pendrin lowers blood pressure in mice.

Francesco Trepiccione, Christelle Soukaseum, Veronique Baudrie, Yusuke Kumai, Jacques Teulon, Bruno Villoutreix, Nicolas Cornière, Philine Wangemann, Andrew J Griffith, Yoon Byung Choi and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2017. 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
1.6field-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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Novel functions of the anion exchanger AE4 (SLC4A9).Pflugers Archiv : European journal of physiology · 2024
    Review
  4. Pendrin: linking acid base to blood pressure.Pflugers Archiv : European journal of physiology · 2024
    Review
  5. Article
  6. SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. NBCe2 (Frontiers in physiology · 2020
    Article
  15. Evaluation of the pathophysiological mechanisms of salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    Review
  16. Article
  17. Aldosterone Is Essential for Angiotensin II-Induced Upregulation of Pendrin.Journal of the American Society of Nephrology : JASN · 2018
    Article
  18. Article
  19. New Findings on the Pathogenesis of Distal Renal Tubular Acidosis.Kidney diseases (Basel, Switzerland) · 2017
    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

13 authors at 6 institutions in 2 countries.

Francesco TrepiccioneINSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
Christelle SoukaseumINSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
Veronique BaudrieINSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
Yusuke KumaiINSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
Jacques TeulonCNRS ERL 8228, INSERM UMRS 1138, Université Pierre et Marie Curie, Centre de Recherche des Cordeliers, Paris, France.
Bruno VilloutreixINSERM U973, MTi-Bioinformatics; University Paris Diderot, Paris, France.
Nicolas CornièreService d'Explorations Fonctionnelles Rénales, Hôpital Felix Guyon, CHU de la Réunion, St Denis, Ile de la Réunion, France.
Philine WangemannAnatomy and Physiology Department, Kansas State University, Manhattan, KS, USA.
Andrew J GriffithOtolaryngology Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
Yoon Byung ChoiOtolaryngology Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
Juliette HadchouelINSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
Regine ChambreyINSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
Dominique EladariService d'Explorations Fonctionnelles Rénales, Hôpital Felix Guyon, CHU de la Réunion, St Denis, Ile de la Réunion, France.
Délégation Paris 5 · FRCentre Hospitalier Universitaire de La Réunion · FRNational Institutes of Health · USCentre National de la Recherche Scientifique · FRInserm · FRKansas State University · US

Funding

Molecular Analysis Of Human Hereditary DeafnessZIADC000060 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI ROUX, ISABELLE · 2009 to 2022
$18.4M
Molecular Analysis Of Human Hereditary DeafnessZ01DC000060 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI GRIFFITH, ANDREW J · 2001 to 2008
$3.0M
Fluid transport in inner ear developmentR01DC012151 · NIDCD · KANSAS STATE UNIVERSITY · PI WANGEMANN, A. PHILINE · 2012 to 2016
$1.9M
Intramural NIH HHS Z01 DC000060NIDCD NIH HHS R01 DC012151
6 · The paper itself

Abstract

backgroundPendrin, the chloride/bicarbonate exchanger of β-intercalated cells of the renal connecting tubule and the collecting duct, plays a key role in NaCl reabsorption by the distal nephron. Therefore, pendrin may be important for the control of extracellular fluid volume and blood pressure.

methodsHere, we have used a genetic mouse model in which the expression of pendrin can be switched-on in vivo by the administration of doxycycline. Pendrin can also be rapidly removed when doxycycline administration is discontinued. Therefore, our genetic strategy allows us to test selectively the acute effects of loss of pendrin function.

resultsWe show that acute loss of pendrin leads to a significant decrease of blood pressure. In addition, acute ablation of pendrin did not alter significantly the acid-base status or blood K +  concentration.

conclusionBy using a transgenic mouse model, avoiding off-target effects related to pharmacological compounds, this study suggests that pendrin could be a novel target to treat hypertension.

Indexed as

AnimalsAnion Transport ProteinsBlood PressureHypertensionMaleMiceMice, TransgenicSulfate TransportersAnion Transport ProteinsSlc26a4 protein, mouseSulfate Transporterschloridediureticshypertensionintercalated cellspendrin

Identifiers

PMID28064162
PMCPMC5837383
OpenAlexW2570753796

What OpenQuestion holds

Textmetadata
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.