Evidence map›Paper›PMID 29895697›Full record

ArticleThe Journal of cell biology2018

Centrosome amplification disrupts renal development and causes cystogenesis.

Lai Kuan Dionne, Kyuhwan Shim, Masato Hoshi, Tao Cheng, Jinzhi Wang, Veronique Marthiens, Amanda Knoten, Renata Basto, Sanjay Jain, Moe R Mahjoub

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  5. The roles of centrosome amplification in diabetes-associated diseases.Frontiers in cell and developmental biology · 2026
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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.

Lai Kuan DionneDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0003-0403-7452
Kyuhwan ShimDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.
Masato HoshiDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0003-2874-1807
Tao ChengDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0003-2771-8584
Jinzhi WangDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.
Veronique MarthiensCentre National de la Recherche Scientifique-Institute Curie, Paris, France.
Amanda KnotenDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.
Renata BastoCentre National de la Recherche Scientifique-Institute Curie, Paris, France.ORCID 0000-0001-5556-2770
Sanjay JainDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0003-2804-127X
Moe R MahjoubDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO mmahjoub@wustl.edu.ORCID 0000-0001-8129-7464
Washington University in St. Louis · USInstitut Curie · FR

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Clay F. Semenkovich · 2013 to 2026
$27.1M
RENAL DISEASET32DK007126 · NIDDK · WASHINGTON UNIVERSITY · PI HUMPHREYS, BENJAMIN D. · 1986 to 2022
$5.2M
Washington University Center for Kidney Disease ResearchP30DK079333 · NIDDK · WASHINGTON UNIVERSITY · PI HAMMERMAN, MARC RANDALL · 2007 to 2011
$5.1M
NOVEL MECHANISMS REGULATING LOWER URINARY TRACT DEVELOPMENT AND INNERVATIONR01DK082531 · NIDDK · WASHINGTON UNIVERSITY · PI JAIN, SANJAY · 2009 to 2018
$3.3M
CENTROSOME DYSFUNCTION IN POLYCYSTIC KIDNEY DISEASER01DK108005 · NIDDK · WASHINGTON UNIVERSITY · PI MAHJOUB, MOHAMED REZA · 2016 to 2020
$1.7M
NIDDK NIH HHS P30 DK079333NIDDK NIH HHS R01 DK082531NIDDK NIH HHS R01 DK108005NIDDK NIH HHS T32 DK007126
6 · The paper itself

Abstract

Centrosome number is tightly controlled to ensure proper ciliogenesis, mitotic spindle assembly, and cellular homeostasis. Centrosome amplification (the formation of excess centrosomes) has been noted in renal cells of patients and animal models of various types of cystic kidney disease. Whether this defect plays a causal role in cystogenesis remains unknown. Here, we investigate the consequences of centrosome amplification during kidney development, homeostasis, and after injury. Increasing centrosome number in vivo perturbed proliferation and differentiation of renal progenitors, resulting in defective branching morphogenesis and renal hypoplasia. Centrosome amplification disrupted mitotic spindle morphology, ciliary assembly, and signaling pathways essential for the function of renal progenitors, highlighting the mechanisms underlying the developmental defects. Importantly, centrosome amplification was sufficient to induce rapid cystogenesis shortly after birth. Finally, we discovered that centrosome amplification sensitized kidneys in adult mice, causing cystogenesis after ischemic renal injury. Our study defines a new mechanism underlying the pathogenesis of renal cystogenesis, and identifies a potentially new cellular target for therapy.

Indexed as

AnimalsCell DifferentiationCell ProliferationCentrosomeEpithelial CellsHomeostasisHumansKidneyMiceMitosisMorphogenesisSpindle Apparatus

Identifiers

PMID29895697
PMCPMC6028550
OpenAlexW2808065882

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.