Evidence map›Paper›PMID 21146605›Full record

ReviewBiochimica et biophysica acta2011

Polycystic kidney disease: pathogenesis and potential therapies.

Vinita Takiar, Michael J Caplan

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Predictors of autosomal dominant polycystic kidney disease progression.Journal of the American Society of Nephrology : JASN · 2014
    Pooled it
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  15. Aquaporin-3 deficiency slows cyst enlargement in experimental mouse models of autosomal dominant polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
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  19. Three-dimensional in vitro models answer the right questions in ADPKD cystogenesis.American journal of physiology. Renal physiology · 2018
    Review
  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

2 authors at 1 institution in 1 country.

Vinita TakiarDepartment of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA.
Michael J Caplan
Yale University · US

Funding

YALE CENTER FOR THE STUDY OF POLYCYSTIC KIDNEY DISEASEP50DK057328 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 1999 to 2009
$11.1M
Center for Polycystic Kidney Disease Research at YaleP30DK090744 · NIDDK · YALE UNIVERSITY · PI CAPLAN, MICHAEL J. · 2010 to 2014
$5.6M
NIDDK NIH HHS DK-57328NIDDK NIH HHS P30 DK090744NIDDK NIH HHS P50 DK057328
6 · The paper itself

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is a prevalent, inherited condition for which there is currently no effective specific clinical therapy. The disease is characterized by the progressive development of fluid-filled cysts derived from renal tubular epithelial cells which gradually compress the parenchyma and compromise renal function. Current interests in the field focus on understanding and exploiting signaling mechanisms underlying disease pathogenesis as well as delineating the role of the primary cilium in cystogenesis. This review highlights the pathogenetic pathways underlying renal cyst formation as well as novel therapeutic targets for the treatment of PKD. This article is part of a Special Issue entitled: Polycystic Kidney Disease.

Indexed as

AnimalsCiliaCyclic AMPCyst FluidHumansPolycystic Kidney, Autosomal DominantSignal TransductionTRPP Cation ChannelsCyclic AMPTRPP Cation Channels

Identifiers

PMID21146605
PMCPMC3139769
OpenAlexW2152299918

What OpenQuestion holds

Textmetadata
LicenceTDM
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.