Evidence map›Paper›PMID 31570523›Full record

ArticleThe Journal of biological chemistry2019

Pharmacological reversal of renal cysts from secretion to absorption suggests a potential therapeutic strategy for managing autosomal dominant polycystic kidney disease.

Murali K Yanda, Boyoung Cha, Cristina V Cebotaru, Liudmila Cebotaru

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Ameliorating liver disease in an autosomal recessive polycystic kidney disease mouse model.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  7. Review
  8. The Mitochondrial CaCell calcium · 2022
    Article
  9. Review
  10. Review
  11. VX-809 mitigates disease in a mouse model of autosomal dominant polycystic kidney disease bearing the R3277C human mutation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. The chloride channel CFTR is not required for cyst growth in an ADPKD mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    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

4 authors at 2 institutions in 1 country.

Murali K YandaDepartment of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.ORCID 0000-0002-4913-470X
Boyoung ChaDepartment of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Cristina V CebotaruDepartment of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Liudmila CebotaruDepartment of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 lcebotaru@jhmi.edu.ORCID 0000-0002-4362-8995
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2008 to 2022
$16.8M
Translational Research Enhancement CoreP30DK089502 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI ZACHOS, NICHOLAS CONSTANTINE · 2011 to 2020
$12.0M
LSM880 Laser-scanning Microscope with Airyscan ModuleS10OD023548 · OD · JOHNS HOPKINS UNIVERSITY · PI KUO, SCOT CHARLES · 2018 to 2018
$439k
NIDDK NIH HHS P30 DK079310NIDDK NIH HHS P30 DK089502NIH HHS S10 OD023548
6 · The paper itself

Abstract

Autosomal-dominant polycystic kidney disease (ADPKD) induces a secretory phenotype, resulting in multiple fluid-filled cysts. We have previously demonstrated that VX-809, a corrector of the cystic fibrosis transmembrane conductance regulator (CFTR), reduces cyst growth. Here, we show that in normal mice CFTR is located within the cells and also at the apical and basolateral membranes. However, in polycystic kidney disease (

Indexed as

Absorption, PhysicochemicalAminopyridinesBenzodioxolesCystic Fibrosis Transmembrane Conductance RegulatorCystsEndoplasmic ReticulumGolgi ApparatusHumansPolycystic Kidney, Autosomal DominantProtein TransportSodium-Hydrogen Exchanger 3AminopyridinesBenzodioxolesCystic Fibrosis Transmembrane Conductance RegulatorlumacaftorSLC9A3 protein, humanSodium-Hydrogen Exchanger 3chloride transportcystic fibrosis transmembrane conductance regulator (CFTR)epithelial sodium channel (ENaC)ion channelkidneyprotein targetingrenal physiologysodium channelsodium–proton exchange

Identifiers

PMID31570523
PMCPMC6851297
OpenAlexW2987647754

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.