Evidence map›Paper›PMID 34635846›Full record

ArticleNature genetics2021

Renal plasticity revealed through reversal of polycystic kidney disease in mice.

Ke Dong, Chao Zhang, Xin Tian, Daniel Coman, Fahmeed Hyder, Ming Ma, Stefan Somlo

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
14.5field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 116 citations in OpenAlex.

  1. Trial
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  9. Article
  10. Collecting Duct-Targeted Lipid Nanoparticles DeliverbioRxiv : the preprint server for biology · 2026
    Article
  11. A Ciliary Phosphoinositide Pathway Regulates the Dosage of Polycystins in Primary Cilia.Journal of the American Society of Nephrology : JASN · 2026
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. In vivo base editing reduces liver cysts in autosomal dominant polycystic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  20. Article

11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Ke DongDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Chao ZhangDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Xin TianDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Daniel ComanDepartment of Radiology and Biomedical Imaging, Yale School of Medicine, New Haven, CT, USA.
Fahmeed HyderDepartment of Radiology and Biomedical Imaging, Yale School of Medicine, New Haven, CT, USA.
Ming MaDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Stefan SomloDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA. stefan.somlo@yale.edu.ORCID http://orcid.org/0000-0001-5062-4629
Yale University · US

Funding

Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2008 to 2022
$16.8M
Polycystin Dependent Mechanisms of Tubular PlasticityR01DK121948 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2019 to 2023
$2.4M
A forward genetic screen for PKD pathways in mice using the PiggyBac transposonRC1DK086738 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2010 to 2010
$500k
NIDDK NIH HHS P30 DK079310NIDDK NIH HHS R01 DK121948NIDDK NIH HHS RC1 DK086738
6 · The paper itself

Abstract

Initiation of cyst formation in autosomal dominant polycystic kidney disease (ADPKD) occurs when kidney tubule cells are rendered null for either PKD1 or PKD2 by somatic 'second hit' mutations. Subsequent cyst progression remodels the organ through changes in tubule cell shape, proliferation and secretion. The kidney develops inflammation and fibrosis. We constructed a mouse model in which adult inactivation of either Pkd gene can be followed by reactivation of the gene at a later time. Using this model, we show that re-expression of Pkd genes in cystic kidneys results in rapid reversal of ADPKD. Cyst cell proliferation is reduced, autophagy is activated and cystic tubules with expanded lumina lined by squamoid cells revert to normal lumina lined by cuboidal cells. Increases in inflammation, extracellular matrix deposition and myofibroblast activation are reversed, and the kidneys become smaller. We conclude that phenotypic features of ADPKD are reversible and that the kidney has an unexpected capacity for plasticity controlled at least in part by ADPKD gene function.

Indexed as

Adaptation, PhysiologicalAnimalsCell PlasticityFemaleFibrosisGene SilencingGenetic TherapyKidneyMaleMiceMice, Inbred C57BLPolycystic Kidney DiseasesProtein Kinase CTranscriptional ActivationTRPP Cation ChannelsProtein Kinase Cprotein kinase DTRPP Cation Channels

Identifiers

PMID34635846
PMCPMC9278957
OpenAlexW3205609245

What OpenQuestion holds

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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.