Evidence map›Paper›PMID 23095233›Full record

ArticleNephron. Experimental nephrology2012

A novel mouse model of podocyte depletion.

L Wang, Y Tang, D N Howell, P Ruiz, R F Spurney

Open access · bronzeAbstract read
In one paragraph

Article in Nephron. Experimental nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Can podocytes be regenerated in adults?Current opinion in nephrology and hypertension · 2017
    Review
  4. Article
  5. Review
  6. Article
  7. Augmenting podocyte injury promotes advanced diabetic kidney disease in Akita mice.Biochemical and biophysical research communications · 2014
    Article
  8. 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

5 authors at 1 institution in 1 country.

L WangDivision of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, NC 27710, USA. spurn002 @ mc.duke.edu
Y Tang
D N Howell
P Ruiz
R F Spurney
Duke University · US

Funding

Role of Gq Signaling in Promoting Podocyte Injury in Diabetes MellitusR01DK087707 · NIDDK · DUKE UNIVERSITY · PI SPURNEY, ROBERT · 2011 to 2014
$1.4M
A Novel Mouse Model of Podocyte InjuryR01DK075688 · NIDDK · DUKE UNIVERSITY · PI SPURNEY, ROBERT · 2009 to 2011
$1.2M
NIDDK NIH HHS 3R01DK075688-01A2S1NIDDK NIH HHS R01 DK075688NIDDK NIH HHS R01-DK075688NIDDK NIH HHS R01 DK087707NIDDK NIH HHS R01-DK087707
6 · The paper itself

Abstract

aimThe goal of this study was to examine the capacity for glomerular repair after a podocyte-depleting injury.

methodsWe created transgenic (TG) mice expressing the yeast enzyme cytosine deaminase specifically in glomerular podocytes. In these TG animals, the prodrug 5-flucytosine (5-FC) is converted to 5-fluorouracil and promotes cell death.

resultsTreatment with increasing dosages of 5-FC caused graded increases in proteinuria 1-2 weeks after treatment, which returned to control levels by the 10-week time point. Light microscopic examination revealed minimal pathology at the 2-week time point, but electron microscopy revealed found foot process effacement as well as focal areas of glomerular basement membrane duplication, and immunohistochemical studies detected podocyte apoptosis and a decrease in the number of Wilms' tumor protein 1 (WT1)-positive cells. By the 10-week time point, however, the number of WT1-positive cells was similar to controls and a few mice had developed focal areas of glomerulosclerosis. Consistent with the effects of 5-FC on podocyte number, expression of the podocyte mRNAs for nephrin, podocin, synaptopodin and podocalyxin were altered in a similar temporal fashion.

conclusionThe glomerulus has a significant capacity for repair after a podocyte-depleting injury.

Indexed as

Disease Models, AnimalAcute Kidney InjuryAnimalsAntimetabolitesCytosine DeaminaseFlucytosineHumansKidneyMiceMice, TransgenicPodocytesProteinuriaRecovery of FunctionAntimetabolitesCytosine DeaminaseFlucytosine

Identifiers

PMID23095233
PMCPMC3574644
OpenAlexW2170159891

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.