Evidence map›Paper›PMID 24511118›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

MicroRNA-17~92 is required for nephrogenesis and renal function.

April K Marrone, Donna B Stolz, Sheldon I Bastacky, Dennis Kostka, Andrew J Bodnar, Jacqueline Ho

Open access · bronzeAbstract read
In one paragraph

Article 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 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.6field-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

50 citing papers in PubMed, 76 citations in OpenAlex.

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  15. Non-Coding RNAs in Hereditary Kidney Disorders.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Epigenetic regulation of kidney progenitor cells.Stem cells translational medicine · 2020
    Review
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

6 authors at 2 institutions in 1 country.

April K MarroneDivision of Nephrology, Department of Pediatrics.
Donna B StolzDepartment of Cell Biology.
Sheldon I BastackyDepartment of Pathology, and University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Dennis KostkaDepartments of Developmental Biology and Computational Systems Biology, University of Pittsburgh School of Medicine, and.
Andrew J BodnarDivision of Nephrology, Department of Pediatrics.
Jacqueline HoDivision of Nephrology, Department of Pediatrics, jacqueline.ho2@chp.edu.
University of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CARATTINO, MARCELO DANIEL · 2008 to 2022
$13.4M
MicroRNAs in Kidney Progenitor Cells.R00DK087922 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HO, JACQUELINE · 2012 to 2014
$722k
MicroRNAs in kidney progenitor cells.K99DK087922 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HO, JACQUELINE · 2010 to 2011
$216k
NIDDK NIH HHS DK087922NIDDK NIH HHS K99 DK087922NIDDK NIH HHS P30 DK079307NIDDK NIH HHS P30-DK079307NIDDK NIH HHS R00 DK087922
6 · The paper itself

Abstract

Deletion of all microRNAs (miRNAs) in nephron progenitors leads to premature loss of these cells, but the roles of specific miRNAs in progenitors have not been identified. Deletions in the MIR17HG cluster (miR-17~92 in mice), detected in a subset of patients with Feingold syndrome, represent the first miRNA mutations to be associated with a developmental defect in humans. Although MIR17HG is expressed in the developing kidney, and patients with Feingold syndrome caused by MYCN mutations have renal anomalies, it remains unclear to what extent MIR17HG contributes to renal development and function. To define the role of miR-17~92, we generated mice with a conditional deletion of miR-17~92 in nephron progenitors and their derivatives. The nephron progenitor population was preserved in these mice; however, this deletion impaired progenitor cell proliferation and reduced the number of developing nephrons. Postnatally, mutant mice developed signs of renal disease, including albuminuria by 6 weeks and focal podocyte foot process effacement and glomerulosclerosis at 3 months. Taken together, these data support a role for this miRNA cluster in renal development, specifically in the regulation of nephron development, with subsequent consequences for renal function in adult mice.

Indexed as

AnimalsFemaleKidneyMaleMiceMicroRNAsNephronsOrganogenesisRenal Insufficiency, ChronicMicroRNAsMIRN17-92 microRNA, mousegenetic renal diseasegenetics and developmentnephron

Identifiers

PMID24511118
PMCPMC4073423
OpenAlexW2153152718

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.