Evidence map›Paper›PMID 21067510›Full record

ReviewCurrent diabetes reviews2011

The glomerular podocyte as a target of growth hormone action: implications for the pathogenesis of diabetic nephropathy.

P Anil Kumar, Frank C Brosius, Ram K Menon

Open access · greenAbstract readReview
In one paragraph

Review in Current diabetes reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  3. Review
  4. Review
  5. Renal effects of growth hormone in health and in kidney disease.Pediatric nephrology (Berlin, Germany) · 2021
    Article
  6. Article
  7. Article
  8. The effects of growth hormone on therapy resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2019
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Glomerular endothelial cell injury and cross talk in diabetic kidney disease.American journal of physiology. Renal physiology · 2015
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

P Anil KumarPediatrics & Communicable Diseases, University of Michigan, Ann Arbor, MI 48109-0718, USA.
Frank C Brosius
Ram K Menon
Pediatrics and Genetics · US

Funding

PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Integrated Systems Biology Approach to Diabetic Microvascular ComplicationsR24DK082841 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABCOUWER, STEVEN F, BROSIUS, FRANK C · 2008 to 2020
$13.1M
Mouse Models of Diabetic Nephropathy and NeuropathyU01DK060994 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROSIUS, FRANK C · 2001 to 2005
$3.3M
Fetal/Postnatal Regulation of GH Receptor ExpressionR01DK049845 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MENON, RAM K. · 2002 to 2010
$2.2M
FETAL/POSTNATAL REGULATION OF GH RECEPTOR EXPRESSIONR29DK049845 · NIDDK · CHILDREN'S HOSP PITTSBURGH/UPMC HLTH SYS · PI MENON, RAM K. · 1996 to 2000
$109k
Fetal/Postnatal Regulation of Expression of the GH ReceptorR56DK049845 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MENON, RAM K. · 2006 to 2006
$72k
NIDDK NIH HHS DK49845NIDDK NIH HHS P60 DK020572NIDDK NIH HHS P60DK-20572NIDDK NIH HHS R01 DK049845NIDDK NIH HHS R24 DK082841NIDDK NIH HHS R29 DK049845NIDDK NIH HHS R56 DK049845NIDDK NIH HHS U01 DK060994
6 · The paper itself

Abstract

Involvement of the growth hormone (GH) / insulin-like growth factor 1 (IGF-I) axis in the pathogenesis of diabetic nephropathy (DN) is strongly suggested by studies investigating the impact of GH excess and deficiency on renal structure and function. GH excess in both the human (acromegaly) and in transgenic animal models is characterized by significant structural and functional changes in the kidney. In the human a direct relationship has been noted between the activity of the GH/IGF-1 axis and renal hypertrophy, microalbuminuria, and glomerulosclerosis. Conversely, states of GH deficiency or deficiency or inhibition of GH receptor (GHR) activity confer a protective effect against DN. The glomerular podocyte plays a central and critical role in the structural and functional integrity of the glomerular filtration barrier and maintenance of normal renal function. Recent studies have revealed that the glomerular podocyte is a target of GH action and that GH's actions on the podocyte could be detrimental to the structure and function of the podocyte. These results provide a novel mechanism for GH's role in the pathogenesis of DN and offer the possibility of targeting the GH/IGF-1 axis for the prevention and treatment of DN.

Indexed as

AnimalsDiabetic NephropathiesDisease ProgressionHuman Growth HormoneHumansInsulin-Like Growth Factor IKidney GlomerulusModels, BiologicalPodocytesReceptors, SomatotropinHuman Growth HormoneInsulin-Like Growth Factor IReceptors, Somatotropin

Identifiers

PMID21067510
PMCPMC4007067
OpenAlexW2132130814

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.