Evidence map›Paper›PMID 32554753›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Epithelial Vasopressin Type-2 Receptors Regulate Myofibroblasts by a YAP-CCN2-Dependent Mechanism in Polycystic Kidney Disease.

Nidhi Dwivedi, Shixin Tao, Abeda Jamadar, Sonali Sinha, Christianna Howard, Darren P Wallace, Timothy A Fields, Andrew Leask, James P Calvet, Reena Rao

Open access · bronzeAbstract 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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  14. Generation of Conditional KO Mice of CCN2 and Its Function in the Kidney.Methods in molecular biology (Clifton, N.J.) · 2023
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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

10 authors at 2 institutions in 2 countries.

Nidhi DwivediThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Shixin TaoThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.ORCID 0000-0001-5757-7407
Abeda JamadarThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Sonali SinhaThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Christianna HowardThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Darren P WallaceThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.ORCID 0000-0003-4616-7669
Timothy A FieldsThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Andrew LeaskSchool of Dentistry, University of Saskatchewan, Saskatoon, SK, Canada.
James P CalvetThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas.
Reena RaoThe Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas rrao@kumc.edu.ORCID 0000-0003-0739-9344
University of Kansas Medical Center · USUniversity of Saskatchewan · CA

Funding

Center for Polycystic Kidney Disease Research at YaleP30DK090744 · NIDDK · YALE UNIVERSITY · PI CAPLAN, MICHAEL J. · 2010 to 2014
$5.6M
Pilot and Feasibility CoreP30DK106912 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CALVET, JAMES P · 2015 to 2019
$5.5M
Regulation of Renal Response to Vasopressin by Glycogen SynthaseR01DK083525 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI RAO, REENA · 2011 to 2020
$2.5M
NIDDK NIH HHS P30 DK090744NIDDK NIH HHS P30 DK106912NIDDK NIH HHS R01 DK083525
6 · The paper itself

Abstract

backgroundFibrosis is a major cause of loss of renal function in autosomal dominant polycystic kidney disease (ADPKD). In this study, we examined whether vasopressin type-2 receptor (V2R) activity in cystic epithelial cells can stimulate interstitial myofibroblasts and fibrosis in ADPKD kidneys.

methodsWe treated

resultsV2R stimulation using dDAVP increased the renal interstitial myofibroblast population and ECM deposition. Similarly, conditioned media from human ADPKD cystic epithelial cells increased myofibroblast activation

conclusionsOur results demonstrate a novel mechanism by which cystic epithelial cells stimulate myofibroblasts in the pericystic microenvironment, leading to fibrosis in ADPKD. The V2R-YAP-CCN2 cell signaling pathway may present a potential therapeutic target for fibrosis in ADPKD.

Indexed as

AnimalsCell Cycle ProteinsConnective Tissue Growth FactorDeamino Arginine VasopressinExtracellular MatrixFibrosisHumansKidneyMiceMyofibroblastsPolycystic Kidney, Autosomal DominantReceptors, VasopressinTranscription FactorsTRPP Cation ChannelsCell Cycle ProteinsConnective Tissue Growth FactorDeamino Arginine VasopressinReceptors, VasopressinTranscription FactorsTRPP Cation ChannelsYY1AP1 protein, humanpolycystic kidney diseaserenal fibrosisvasopressin receptor

Identifiers

PMID32554753
PMCPMC7460894
OpenAlexW3036096954

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.