Evidence map›Paper›PMID 25415617›Full record

ArticleCurrent opinion in nephrology and hypertension2015

Insulin signaling: implications for podocyte biology in diabetic kidney disease.

Richard Coward, Alessia Fornoni

Abstract read
In one paragraph

Article in Current opinion in nephrology and hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Obesity-Related Kidney Disease: A Growing Threat to Renal Health.International journal of molecular sciences · 2025
    Review
  4. Obesity-Related Glomerulosclerosis-How Adiposity Damages the Kidneys.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Acute kidney injury in diabetes mellitus: Epidemiology, diagnostic, and therapeutic concepts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Lipid mediators of insulin signaling in diabetic kidney disease.American journal of physiology. Renal physiology · 2019
    Review
  19. Article
  20. Prompt apoptotic response to high glucose in SGLT-expressing renal cells.American journal of physiology. Renal physiology · 2019
    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

2 authors at 2 institutions in 2 countries.

Richard CowardaChildren's Renal Unit, University of Bristol, Bristol Royal Hospital for Children, Bristol, UK bKatz Family Drug Discovery Center and Division of Nephrology and Hypertension, University of Miami, Miller School of Medicine, Miami, Florida, USA.
Alessia Fornoni
Bristol Royal Hospital for Children · GBUniversity of Miami · US

Funding

Miami Clinical and Translational Science InstituteUL1TR000460 · NCATS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SACCO, RALPH L. · 2012 to 2016
$16.9M
Crosstalk Between Lipid Droplets and Other Organelles in PodocytesR01DK104753 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2015 to 2025
$5.9M
Novel Targets of Rituximab in FSGSR01DK090316 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2011 to 2015
$1.7M
Medical Research Council MR/K010492/1NCATS NIH HHS 1UL1TR000460NCATS NIH HHS UL1 TR000460NIDDK NIH HHS DK090316NIDDK NIH HHS R01 DK090316NIDDK NIH HHS R01 DK104753PHS HHS 5U24DX076169
6 · The paper itself

Abstract

purpose of reviewSeveral key elements of the insulin signaling cascade contribute to podocyte function and survival. While it was initially thought that the consequences of altered insulin signaling to podocyte function was strictly related to altered glucose uptake, it has become clear that upstream signaling events involved in cell survival, lipid metabolism or nutrient sensing and modulated by insulin are strong independent contributors to podocyte function. RECENT

findingsAkt2, the major isoform of Akt activated following cellular insulin stimulation, protects against the progression of renal disease in nephron-deficient mice, and podocyte-specific deletion of Akt2 results in a more rapid progression of experimental glomerular disease. In diabetes, podocyte mammalian target of rapamycin activation clearly contributes to podocyte injury and regulated autophagy. Furthermore, podocyte-specific glucose transporter type 4 (GLUT4) deficiency protects podocytes by preventing mammalian target of rapamycin signaling independently of glucose uptake. Finally, intracellular lipids have been recently recognized as major modulators of podocyte insulin signaling and as a new therapeutic target. SUMMARY: The identification of new contributors to podocyte insulin signaling is of extreme translational value as it may lead to new drug development strategies for diabetic kidney disease, as well as for other proteinuric kidney diseases.

Indexed as

Signal TransductionAnimalsAutophagyCell MembraneCell SurvivalCholesterolDiabetic NephropathiesGlucose Transporter Type 4HumansInsulinPodocytesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCholesterolGlucose Transporter Type 4InsulinProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID25415617
PMCPMC4386894
OpenAlexW2069477355

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.