Evidence map›Paper›PMID 26104383›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2015

Nox2 is a mediator of ischemia reperfusion injury.

A S Karim, S R Reese, N A Wilson, L M Jacobson, W Zhong, A Djamali

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of reactive oxygen species and oxidative stress in the pathomechanism of glaucoma.Medical hypothesis, discovery & innovation ophthalmology journal · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Gene knockout of the NaAmerican journal of physiology. Renal physiology · 2020
    Article
  11. NOX2 is involved in CB2-mediated protection against lung ischemia-reperfusion injury in mice.International journal of clinical and experimental pathology · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

A S KarimSchool of Medicine and Public Health, University of Wisconsin, Madison, WI.
S R ReeseDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
N A WilsonDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
L M JacobsonDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
W ZhongDepartment of Pathology and Laboratory Medicine, University of Wisconsin, Madison, WI.
A DjamaliSchool of Medicine and Public Health, University of Wisconsin, Madison, WI.
University of Wisconsin–Madison · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
The role of Nox2 in CNI-induced renal fibrosisR01DK092454 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI DJAMALI, ARJANG · 2011 to 2015
$1.7M
NIDDK NIH HHS 5R01DK092454-04NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK092454
6 · The paper itself

Abstract

Delayed graft function (DGF) results from ischemia-reperfusion injury (IRI) and the generation of reactive oxygen species. We hypothesized that NADPH oxidase 2 (Nox2) plays an important role in pathways leading to DGF. We tested this hypothesis in vitro, in an animal model of IRI using wild type and Nox2(-/-) mice, and in patients with DGF. Under hypoxic conditions, primary tubular epithelial cells from Nox2(-/-) mice had reduced expression of MMP2, vimentin, and HSP27. BUN and creatinine levels were significantly increased in both Nox2(-/-) and WT mice at 4 weeks and 6 months after IRI, suggesting the development of acute and chronic kidney injury. At 4 weeks, kidney fibrosis (α-SMA, picrosirius) and oxidative stress (dihydroethidine, HNE) were significantly reduced in Nox2(-/-) mice, confirming the oxidative and pro-fibrotic effects of Nox2. The molecular signature of IRI using genomic analyses demonstrated a significant decline in hypoxia reponse, oxidative stress, fibrosis, and inflammation in Nox2(-/-) mice. Immunohistochemical analyses of pre-implanatation kidney allograft biopsies from patients with subsequent DGF showed significantly greater Nox2 levels and vascular injury compared with patients without DGF. These studies demonstrate that Nox2 is a modulator of IRI and its absence is associated with reduced inflammation, OS, and fibrosis.

Indexed as

Analysis of VarianceAnimalsBiomarkersCase-Control StudiesDelayed Graft FunctionDisease Models, AnimalFemaleFibrosisHumansImmunoblottingImmunohistochemistryKidney Function TestsKidney TransplantationMaleMembrane GlycoproteinsMiceBiomarkersCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesReactive Oxygen SpeciesRNA, Small Interferinganimal models: murinekidney (allograft) function/dysfunction

Identifiers

PMID26104383
PMCPMC4636908
OpenAlexW1923914039

What OpenQuestion holds

Textmetadata
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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.