Evidence map›Paper›PMID 23512109›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2013

Role of impaired Nrf2 activation in the pathogenesis of oxidative stress and inflammation in chronic tubulo-interstitial nephropathy.

Mohammad A Aminzadeh, Susanne B Nicholas, Keith C Norris, Nosratola D Vaziri

Open access · bronzeAbstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

78 citing papers in PubMed, 155 citations in OpenAlex.

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18 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

4 authors at 3 institutions in 1 country.

Mohammad A AminzadehDivision of Nephrology and Hypertension, University of California, Irvine, CA, USA.
Susanne B Nicholas
Keith C Norris
Nosratola D Vaziri
University of California, Irvine · USCharles R. Drew University of Medicine and Science · USUniversity of California, Los Angeles · US

Funding

Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Yanyuan Wu · 2012 to 2026
$60.0M
TRAINING COREP20MD000182 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI MILBURN, NORWEETA GERMAINE, SHAPIRO, MARTIN F. · 2002 to 2016
$16.5M
UCLA CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR033176 · NCRR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2011 to 2011
$15.5M
NCRR NIH HHS UL1 RR033176NCRR NIH HHS UL1RR033176NIMHD NIH HHS P20 MD000182NIMHD NIH HHS P20MD000182NIMHD NIH HHS U54 MD007598NIMHD NIH HHS U54MD007598
6 · The paper itself

Abstract

backgroundTubulo-interstitial nephropathy (TIN) is a common cause of chronic kidney disease (CKD). Consumption of an adenine-containing diet causes the accumulation of 2,8-dihydroxyadenine in the renal tubules triggering intense chronic TIN and progressive CKD in rats. CKD in this model is associated with, and largely driven by, oxidative stress and inflammation. Oxidative stress and inflammation in rats with spontaneous focal segmental glomerulosclerosis and rats with CKD induced by 5/6 nephrectomy are associated with an impaired activation of nuclear factor-erythroid-2-related factor 2 (Nrf2) which is the master regulator of genes encoding many antioxidant and detoxifying enzymes. The effect of TIN on the Nrf2 pathway and its key target genes is unknown and was investigated here.

methodsSprague-Dawley rats were randomized to control and adenine-treated (rat chow-containing 0.7% adenine for 2 weeks) groups and followed up for 4 weeks.

resultsThe adenine-treated animals exhibited marked azotemia, impaired urinary concentrating capacity, intense tubular and glomerular damage, interstitial inflammation and fibrosis. This was associated with an increased expression of NAD(P)H oxidase, cyclooxygenase-2 and 12-lipoxygenase, and activation of NF-κB, the master regulator of pro-inflammatory cytokines and chemokines. Oxidative stress and inflammation in the kidneys of adenine-treated animals was accompanied by an impaired activation of Nrf2 and down-regulation of its target gene products including, catalase, heme oxygenase-1 and glutamate-cysteine ligase.

conclusionsChronic TIN is associated with impaired Nrf2 activity which contributes to the pathogenesis of oxidative stress and inflammation and amplifies their damaging effects on the kidney.

Indexed as

Oxidative StressAdenineAnimalsArachidonate 12-LipoxygenaseBlotting, WesternCatalaseChronic DiseaseCyclooxygenase 2Glutamate-Cysteine LigaseHeme Oxygenase-1InflammationMaleNADPH OxidasesNephritis, InterstitialNF-E2-Related Factor 2NF-kappa BAdenineArachidonate 12-LipoxygenaseCatalaseCyclooxygenase 2Glutamate-Cysteine LigaseHeme Oxygenase-1NADPH OxidasesNF-E2-Related Factor 2NF-kappa Bantioxidantschronic kidney diseaseCKD progressionreactive oxygen species

Identifiers

PMID23512109
PMCPMC3765021
OpenAlexW2170419604

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.