Evidence map›Paper›PMID 26908870›Full record

ArticleDiabetes2016

HIF-1 Mediates Renal Fibrosis in OVE26 Type 1 Diabetic Mice.

Bijaya K Nayak, Karthigayan Shanmugasundaram, William E Friedrichs, Rita C Cavaglierii, Mandakini Patel, Jeffrey Barnes, Karen Block

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
4.2field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
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  14. Evolution of hypoxia and hypoxia-inducible factor asparaginyl hydroxylase regulation in chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
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11 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Bijaya K NayakDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
Karthigayan ShanmugasundaramDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
William E FriedrichsDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
Rita C CavaglieriiDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
Mandakini PatelDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
Jeffrey BarnesDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX Audie L. Murphy Memorial VA Hospital Division, South Texas Veterans Health Care System, San Antonio, TX.
Karen BlockDepartment of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX Audie L. Murphy Memorial VA Hospital Division, South Texas Veterans Health Care System, San Antonio, TX block@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · USSouth Texas Veterans Health Care System · US

Funding

INFLAMMATORY MEDIATORS AND GLOMERULAR CELLS IN CULTURER37DK033665 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ABBOUD, HANNA E · 1998 to 2007
$2.1M
Tubular epithelial cell injuryR01DK033665 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GORIN, YVES CLAUDE · 1986 to 2015
$1.3M
NIDDK NIH HHS R01 DK033665NIDDK NIH HHS R37 DK033665
6 · The paper itself

Abstract

Hypoxia-inducible factor (HIF)-1 mediates hypoxia- and chronic kidney disease-induced fibrotic events. Here, we assessed whether HIF-1 blockade attenuates the manifestations of diabetic nephropathy in a type 1 diabetic animal model, OVE26. YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole], an HIF-1 inhibitor, reduced whole kidney glomerular hypertrophy, mesangial matrix expansion, extracellular matrix accumulation, and urinary albumin excretion as well as NOX4 protein expression and NADPH-dependent reactive oxygen species production, while blood glucose levels remained unchanged. The role of NOX oxidases in HIF-1-mediated extracellular matrix accumulation was explored in vitro using glomerular mesangial cells. Through a series of genetic silencing and adenoviral overexpression studies, we have defined GLUT1 as a critical downstream target of HIF-1α mediating high glucose-induced matrix expression through the NADPH oxidase isoform, NOX4. Together, our data suggest that pharmacological inhibition of HIF-1 may improve clinical manifestations of diabetic nephropathy.

Indexed as

AnimalsAntioxidantsCell LineDiabetes Mellitus, Type 1Diabetic NephropathiesExtracellular MatrixFibrosisGene Expression RegulationGlucose Transporter Type 1HyperglycemiaHypoglycemiaHypoglycemic AgentsHypoxia-Inducible Factor 1, alpha SubunitIndazolesKidneyMesangial Cells3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazoleAntioxidantsGlucose Transporter Type 1Hif1a protein, mouseHypoglycemic AgentsHypoxia-Inducible Factor 1, alpha SubunitIndazolesNADPH Oxidase 4NADPH OxidasesNox4 protein, mouseRecombinant ProteinsSlc2a1 protein, mouse

Identifiers

PMID26908870
PMCPMC4839204
OpenAlexW2294795032

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.