Evidence map›Paper›PMID 27601438›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Ibuprofen arginate retains eNOS substrate activity and reverses endothelial dysfunction: implications for the COX-2/ADMA axis.

Nicholas S Kirkby, Abel Tesfai, Blerina Ahmetaj-Shala, Hime H Gashaw, Walkyria Sampaio, Gisele Etelvino, Nádia Miricéia Leão, Robson A Santos, Jane A Mitchell

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-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

3 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

9 authors at 4 institutions in 4 countries.

Nicholas S KirkbyVascular Biology Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; and n.kirkby@imperial.ac.uk.
Abel TesfaiVascular Biology Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; and.
Blerina Ahmetaj-ShalaVascular Biology Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; and.
Hime H GashawVascular Biology Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; and.
Walkyria SampaioDepartment of Physiology and Biophysics, National Institute in Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Gisele EtelvinoDepartment of Physiology and Biophysics, National Institute in Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Nádia Miricéia LeãoDepartment of Physiology and Biophysics, National Institute in Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Robson A SantosDepartment of Physiology and Biophysics, National Institute in Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Jane A MitchellVascular Biology Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; and j.a.mitchell@ic.ac.uk.
Imperial College London · GBNational Institute of Science and Technology · IDUniversidade Federal de Minas Gerais · BRLung Institute · US

Funding

British Heart Foundation FS/16/1/31699Wellcome TrustWellcome Trust 0852551Z108/ZWellcome Trust PS2124
6 · The paper itself

Abstract

Nonsteroidal antiinflammatory drugs, including ibuprofen, are among the most commonly used medications and produce their antiinflammatory effects by blocking cyclooxygenase (COX)-2. Their use is associated with increased risk of heart attacks caused by blocking COX-2 in the vasculature and/or kidney, with our recent work implicating the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormone whose effects can be prevented by l-arginine. The ibuprofen salt ibuprofen arginate (Spididol) was created to increase solubility but we suggest that it could also augment the NO pathway through codelivery of arginine. Here we investigated the idea that ibuprofen arginate can act to simultaneously inhibit COX-2 and preserve the NO pathway. Ibuprofen arginate functioned similarly to ibuprofen sodium for inhibition of mouse/human COX-2, but only ibuprofen arginate served as a substrate for NOS. Ibuprofen arginate but not ibuprofen sodium also reversed the inhibitory effects of ADMA and N

Indexed as

AnimalsArginineCyclooxygenase 2Drug CombinationsEndotheliumEnzyme InhibitorsHumansIbuprofenKidneyMaleMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIISubstrate SpecificityArginineCyclooxygenase 2Drug CombinationsEnzyme InhibitorsIbuprofenibuprofen arginineNitric OxideNitric Oxide Synthase Type IIIN,N-dimethylarginineNOS3 protein, humanNos3 protein, mousePTGS2 protein, humanPtgs2 protein, mouseaspirinmethylargininesnitric oxideprostacyclinVioxx

Identifiers

PMID27601438
PMCPMC5102117
OpenAlexW2529447822

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.