Evidence map›Paper›PMID 31825015›Full record

ArticleFASEB bioAdvances2019

Podocyte GSK3α is important for autophagy and its loss detrimental for glomerular function.

J A Hurcombe, A C Lay, L Ni, A F Barrington, J R Woodgett, S E Quaggin, G I Welsh, R J Coward

Open access · goldAbstract read
In one paragraph

Article in FASEB bioAdvances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. 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

8 authors at 3 institutions in 3 countries.

J A HurcombeBristol Renal, University of Bristol.
A C LayBristol Renal, University of Bristol.
L NiBristol Renal, University of Bristol.
A F BarringtonBristol Renal, University of Bristol.
J R WoodgettLunenfeld-Tanenbaum Research Institute, Sinai Health System & University of Toronto, Canada.
S E QuagginFeinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, Illinois, US.
G I WelshBristol Renal, University of Bristol.
R J CowardBristol Renal, University of Bristol.
University of Bristol · GBNorthwestern University · USUniversity of Toronto · CA

Funding

Therapeutics Development Core (Core B)P30DK114857 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QUAGGIN, SUSAN E. · 2018 to 2022
$5.7M
Medical Research Council MR/K010492/1Medical Research Council MR/T002263/1NIDDK NIH HHS P30 DK114857
6 · The paper itself

Abstract

Podocytes are key cells in maintaining the integrity of the glomerular filtration barrier and preventing albuminuria. Glycogen synthase kinase 3 (GSK3) is a multi-functional serine/threonine kinase existing as two distinct but related isoforms (α and β). In the podocyte it has previously been reported that inhibition of the β isoform is beneficial in attenuating a variety of glomerular disease models but loss of both isoforms is catastrophic. However, it is not known what the role of GSK3α is in these cells. We now show that GSK3α is present and dynamically modulated in podocytes. When GSK3α is transgenically knocked down specifically in the podocytes of mice it causes mild but significant albuminuria by 6-weeks of life. Its loss also does not protect in models of diabetic or Adriamycin-induced nephropathy.

Indexed as

Adriamycin nephropathyalbuminuriaDiabetic nephropathyinsulin signaling

Identifiers

PMID31825015
PMCPMC6902909
OpenAlexW2956079787

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.