Evidence map›Paper›PMID 21543418›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Role of the USF1 transcription factor in diabetic kidney disease.

Amber P Sanchez, JingHong Zhao, Young You, Anne-Emilie Declèves, Maggie Diamond-Stanic, Kumar Sharma

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. TGF-β1-p53 cooperativity regulates a profibrotic genomic program in the kidney: molecular mechanisms and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Adipokines protecting CKD.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2013
    Review
  14. Article
  15. Article
  16. 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

6 authors at 1 institution in 1 country.

Amber P SanchezCenter for Renal Translational Medicine, Division of Nephrology-Hypertension, Department of Medicine, University of California, Veterans Administration San Diego HealthCare System, La Jolla, 92093, USA.
JingHong Zhao
Young You
Anne-Emilie Declèves
Maggie Diamond-Stanic
Kumar Sharma
VA San Diego Healthcare System · US

Funding

Role and Mechanisms of Epithelial Injury in Diabetic NephropathyU01DK060995 · NIDDK · YESHIVA UNIVERSITY · PI BOTTINGER, ERWIN P. · 2001 to 2010
$6.0M
TGF-b signaling in diabetic kidney diseaseR01DK053867 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHARMA, KUMAR · 1999 to 2009
$2.5M
NIDDK NIH HHS R01 DK 053867NIDDK NIH HHS U01 DK 060995NIDDK NIH HHS U01 DK060995
6 · The paper itself

Abstract

The predominant transcription factors regulating key genes in diabetic kidney disease have not been established. The transcription factor upstream stimulatory factor 1 (USF1) is an important regulator of glucose-mediated transforming growth factor (TGF)-β1 expression in mesangial cells; however, its role in the development of diabetic kidney disease has not been evaluated. In the present study, wild-type (WT; USF1 +/+), heterozygous (USF1 +/-), and homozygous (USF1 -/-) knockout mice were intercrossed with Akita mice (Ins2/Akita) to induce type 1 diabetes. Mice were studied up to 36 wk of age. The degree of hyperglycemia and kidney hypertrophy were similar in all groups of diabetic mice; however, the USF1 -/- diabetic mice had significantly less albuminuria and mesangial matrix expansion than the WT diabetic mice. TGF-β1 and renin gene expression and protein were substantially increased in the WT diabetic mice but not in USF1 -/- diabetic mice. The underlying pathway by which USF1 is regulated by high glucose was investigated in mesangial cell culture. High glucose inhibited AMP-activated protein kinase (AMPK) activity and increased USF1 nuclear translocation. Activation of AMPK with AICAR stimulated AMPK activity and reduced nuclear accumulation of USF1. We thus conclude that USF1 is a critical transcription factor regulating diabetic kidney disease and plays a critical role in albuminuria, mesangial matrix accumulation, and TGF-β1 and renin stimulation in diabetic kidney disease. AMPK activity may play a key role in high glucose-induced regulation of USF1.

Indexed as

AlbuminuriaAllelesAMP-Activated Protein KinasesAnimalsCell LineCell NucleusDiabetes Mellitus, Type 1Diabetic NephropathiesDisease ProgressionExtracellular MatrixFemaleHyperglycemiaHypertrophyKidneyMaleMembrane ProteinsAMP-Activated Protein KinasesMembrane ProteinsnephrinRNA, MessengerTransforming Growth Factor betaUpstream Stimulatory FactorsUsf1 protein, mouseUsf2 protein, mouse

Identifiers

PMID21543418
PMCPMC3154594
OpenAlexW2122562390

What OpenQuestion holds

Textmetadata
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.