Evidence map›Paper›PMID 29674687›Full record

ArticleScientific reports2018

Celecoxib exerts protective effects in the vascular endothelium via COX-2-independent activation of AMPK-CREB-Nrf2 signalling.

Fahad Al-Rashed, Damien Calay, Marie Lang, Clare C Thornton, Andrea Bauer, Allan Kiprianos, Dorian O Haskard, Anusha Seneviratne, Joseph J Boyle, Alex H Schönthal and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

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  11. A Novel Pyrazolo[3,4-Molecules and cells · 2022
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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

12 authors at 5 institutions in 3 countries.

Fahad Al-RashedVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Damien CalayVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Marie LangVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Clare C ThorntonVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Andrea BauerVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Allan KiprianosVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Dorian O HaskardVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Anusha SeneviratneVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.
Joseph J BoyleVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0002-4337-3320
Alex H SchönthalDepartment of Molecular Microbiology & Immunology, Keck School of Medicine, University of Southern California, Los Angeles, USA.
Caroline P Wheeler-JonesComparative Biomedical Sciences, The Royal Veterinary College, London, UK.
Justin C MasonVascular Sciences and Rheumatology, Imperial Centre for Translational & Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK. justin.mason@imperial.ac.uk.
Imperial College London · GBKing Saud University · SALung Institute · USRoyal Veterinary College · GBUniversity of Southern California · US

Funding

British Heart Foundation FS/13/12/30037British Heart Foundation PG/11/25/28830British Heart Foundation PG/13/53/30351British Heart Foundation PG/14/45/30906British Heart Foundation PG/16/96/32557
6 · The paper itself

Abstract

Although concern remains about the athero-thrombotic risk posed by cyclo-oxygenase (COX)-2-selective inhibitors, recent data implicates rofecoxib, while celecoxib appears equivalent to NSAIDs naproxen and ibuprofen. We investigated the hypothesis that celecoxib activates AMP kinase (AMPK) signalling to enhance vascular endothelial protection. In human arterial and venous endothelial cells (EC), and in contrast to ibuprofen and naproxen, celecoxib induced the protective protein heme oxygenase-1 (HO-1). Celecoxib derivative 2,5-dimethyl-celecoxib (DMC) which lacks COX-2 inhibition also upregulated HO-1, implicating a COX-2-independent mechanism. Celecoxib activated AMPKα

Indexed as

Adenylate KinaseCelecoxibCyclic AMP Response Element-Binding ProteinCyclooxygenase 2 InhibitorsEndothelium, VascularEnzyme InductionHeme Oxygenase-1HumansHuman Umbilical Vein Endothelial CellsNF-E2-Related Factor 2NF-kappa BPhosphorylationSignal TransductionTumor Necrosis Factor-alphaAdenylate KinaseCelecoxibCREB1 protein, humanCyclic AMP Response Element-Binding ProteinCyclooxygenase 2 InhibitorsHeme Oxygenase-1HMOX1 protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2NF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID29674687
PMCPMC5908847
OpenAlexW2799710621

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.