Evidence map›Paper›PMID 24556353›Full record

ReviewJournal of the American Society of Nephrology : JASN2014

Vasopressin-2 receptor signaling and autosomal dominant polycystic kidney disease: from bench to bedside and back again.

Markus M Rinschen, Bernhard Schermer, Thomas Benzing

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. A Snake Toxin Derivative for Treatment of Hyponatremia and Polycystic Kidney Diseases.Journal of the American Society of Nephrology : JASN · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. The Biology of Vasopressin.Biomedicines · 2021
    Review
  14. Review
  15. Review
  16. Vasopressin Increases Urinary AcidificationJournal of the American Society of Nephrology : JASN · 2019
    Article
  17. Article
  18. Review
  19. N-Degradomic Analysis Reveals a Proteolytic Network Processing the Podocyte Cytoskeleton.Journal of the American Society of Nephrology : JASN · 2017
    Article
  20. 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

3 authors at 1 institution in 1 country.

Markus M RinschenDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, and.
Bernhard SchermerDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, and Systems Biology of Aging Cologne, University of Cologne, Cologne, Germany.
Thomas BenzingDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, and Systems Biology of Aging Cologne, University of Cologne, Cologne, Germany thomas.benzing@uk-koeln.de.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blockade of the vasopressin-2 receptor (V2R) in the kidney has recently emerged as a promising therapeutic strategy in autosomal dominant polycystic kidney disease. The pathophysiologic basis of V2R-dependent cyst proliferation and disease progression, however, is not fully understood. Recent evidence suggests that polycystic kidney disease is characterized by defects in urinary concentrating mechanisms and subsequent deregulation of vasopressin excretion by the neurohypophysis. On the cellular level, several recent studies revealed unexpected crosstalk of signaling pathways downstream of V2R activation in the kidney epithelium. This review summarizes some of the unexpected roles of V2R signaling and suggests that vasopressin signaling itself may contribute crucially to loss of polarity and enhanced proliferation in cystic kidney epithelium.

Indexed as

AnimalsAntidiuretic Hormone Receptor AntagonistsBenzazepinesHumansKidney Tubules, CollectingPolycystic Kidney, Autosomal DominantReceptors, VasopressinSignal TransductionTolvaptanAntidiuretic Hormone Receptor AntagonistsAVPR2 protein, humanBenzazepinesReceptors, VasopressinTolvaptanADPKDCell SignalingCell & Transport Physiologycollecting ductsvasopressin

Identifiers

PMID24556353
PMCPMC4033383
OpenAlexW2115059902

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.