Evidence map›Paper›PMID 20889126›Full record

ArticleCell metabolism2010

Insulin signaling to the glomerular podocyte is critical for normal kidney function.

Gavin I Welsh, Lorna J Hale, Vera Eremina, Marie Jeansson, Yoshiro Maezawa, Rachel Lennon, Deborah A Pons, Rachel J Owen, Simon C Satchell, Mervyn J Miles and 10 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed, 1 pooled it
14.2field-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

239 citing papers in PubMed, 1 synthesis or guideline pooled it, 446 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Short-term changes after a weight reduction intervention in advanced diabetic nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2013
    Trial
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Insulin receptorNature communications · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Metabolic Crosstalk in Diabetic Kidney Disease: Synergistic Effects of Glucotoxicity and Lipotoxicity.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  18. Review
  19. Observational
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 3 countries.

Gavin I WelshAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Lorna J HaleAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Vera EreminaSamuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X5, Canada.
Marie JeanssonSamuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X5, Canada.
Yoshiro MaezawaSamuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X5, Canada.
Rachel LennonAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Deborah A PonsAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Rachel J OwenSchool of Physics, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Simon C SatchellAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Mervyn J MilesSchool of Physics, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Christopher J CauntDepartment of Molecular Pharmacology, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Craig A McArdleDepartment of Molecular Pharmacology, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Hermann PavenstädtDepartment of Internal Medicine D, Nephrology and Hypertension, University Clinics Muenster, Muenster 48149, Germany.
Jeremy M TavaréSchool of Biochemistry, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Andrew M HerzenbergDepartment of Pathology, University Health Network and University of Toronto, Ontario M5G 2C4, Canada.
C Ronald KahnJoslin Diabetes Center and Harvard Medical School, Boston, MA 02215, USA.
Peter W MathiesonAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Susan E QuagginSamuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X5, Canada.
Moin A SaleemAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK.
Richard J M CowardAcademic Renal Unit, School of Clinical Sciences, University of Bristol, Bristol BS8 1TH, UK; Samuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 1X5, Canada. Electronic address: richard.coward@bristol.ac.uk.
University of Bristol · GBLunenfeld-Tanenbaum Research Institute · CAUniversity of Toronto · CAHarvard University · USMount Sinai Hospital · CAUniversity Health Network · CA

Funding

INSULIN RECEPTOR STRUCTURE AND TURNOVERR37DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2000 to 2019
$12.9M
The Insulin Receptor and Its Signaling MechanismsR01DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI C RONALD KAHN · 1986 to 2026
$4.2M
Medical Research Council G0501901Medical Research Council G0800200NIDDK NIH HHS R01 DK031036NIDDK NIH HHS R37 DK031036Wellcome Trust
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is the leading cause of renal failure in the world. It is characterized by albuminuria and abnormal glomerular function and is considered a hyperglycemic "microvascular" complication of diabetes, implying a primary defect in the endothelium. However, we have previously shown that human podocytes have robust responses to insulin. To determine whether insulin signaling in podocytes affects glomerular function in vivo, we generated mice with specific deletion of the insulin receptor from their podocytes. These animals develop significant albuminuria together with histological features that recapitulate DN, but in a normoglycemic environment. Examination of "normal" insulin-responsive podocytes in vivo and in vitro demonstrates that insulin signals through the MAPK and PI3K pathways via the insulin receptor and directly remodels the actin cytoskeleton of this cell. Collectively, this work reveals the critical importance of podocyte insulin sensitivity for kidney function.

Indexed as

AnimalsDiabetic NephropathiesInsulinKidneyKidney GlomerulusMiceMice, KnockoutMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPodocytesReceptor, InsulinSignal TransductionInsulinMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesReceptor, Insulin

Identifiers

PMID20889126
PMCPMC4949331
OpenAlexW2157212924

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.