Evidence map›Paper›PMID 26671967›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy.

Line Nilsson, Kirsten Madsen, Søren Krag, Jørgen Frøkiær, Boye L Jensen, Rikke Nørregaard

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. EPActa physiologica (Oxford, England) · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Activation of the prostaglandin EActa physiologica (Oxford, England) · 2019
    Article
  11. Cell Death in the Kidney.International journal of molecular sciences · 2019
    Review
  12. Article
  13. The molecular biology of pelvi-ureteric junction obstruction.Pediatric nephrology (Berlin, Germany) · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. 15-Deoxy-ΔMediators of inflammation · 2017
    Article
  18. Role of COX-2 in unilateral ureteral obstruction: what is new?American journal of physiology. Renal physiology · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Line NilssonDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark;
Kirsten MadsenCardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark; Department of Pathology, Odense University Hospital, Odense, Denmark.
Søren KragDepartment of Pathology, Aarhus University Hospital, Aarhus, Denmark; and.
Jørgen FrøkiærDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark;
Boye L JensenCardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark;
Rikke NørregaardDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark; rn@clin.au.dk.
Aarhus University · DKAarhus University Hospital · DKOdense University Hospital · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal oxidative stress is increased in response to ureteral obstruction. In vitro, cyclooxygenase (COX)-2 activity contributes to protection against oxidants. In the present study, we tested the hypothesis that COX-2 activity counters oxidative stress and apoptosis in an in vivo model of obstructive nephropathy. Renal oxidative stress markers, antioxidant enzymes, and markers of tubular injury, tubular dilation, and apoptosis were investigated in COX-2 knockout (COX-2(-/-)) and wild-type (WT) mice subjected to 3 or 7 days of unilateral ureteral obstruction (UUO). In a separate series, WT sham-operated and UUO mice were treated with a selective COX-2 inhibitor, parecoxib. COX-2 increased in response to UUO; the oxidative stress markers 4-hydroxynonenal and nitrotyrosine protein residues increased in kidney tissue with no genotype difference after UUO, whereas the antioxidant enzymes heme oxygenase-1 and SOD2 displayed higher levels in COX-2(-/-) mice. Tubular injury was aggravated by COX-2 deletion, as measured by tubular dilatation, an increase in kidney injury molecule-1, cortical caspase-3 content, and apoptosis index. In conclusion, COX-2 is necessary to protect against tubular injury and apoptosis after UUO but not necessary to protect against oxidative stress. COX-2 is not likely to directly regulate antioxidant enzymes heme oxygenase-1 and SOD in the kidney.

Indexed as

ApoptosisAnimalsAntioxidantsCyclooxygenase 2Cyclooxygenase 2 InhibitorsKidney DiseasesMiceMice, KnockoutOxidative StressUreteral ObstructionAntioxidantsCyclooxygenase 2Cyclooxygenase 2 InhibitorsPtgs2 protein, mouseapoptosiscyclooxygenase-2oxidative stressunilateral ureteral obstruction

Identifiers

PMID26671967
PMCPMC4683307
OpenAlexW2264120806

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.