Evidence map›Paper›PMID 29135921›Full record

ReviewAntioxidants (Basel, Switzerland)2017

Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate.

Denise Burtenshaw, Roya Hakimjavadi, Eileen M Redmond, Paul A Cahill

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

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25 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 2 institutions in 2 countries.

Denise BurtenshawVascular Biology & Therapeutics, School of Biotechnology, Dublin City University, D09NR58 Dublin, Ireland. denise.burtenshaw3@mail.dcu.ie.ORCID 0000-0002-5958-1773
Roya HakimjavadiVascular Biology & Therapeutics, School of Biotechnology, Dublin City University, D09NR58 Dublin, Ireland. roya.hakimjavadi@dcu.ie.
Eileen M RedmondDepartment of Surgery (Research), University of Rochester Medical Centre, Rochester, NY 14620, USA. eileen_redmond@urmc.rochester.edu.ORCID 0000-0001-8642-4418
Paul A CahillVascular Biology & Therapeutics, School of Biotechnology, Dublin City University, D09NR58 Dublin, Ireland. paul.cahill@dcu.ie.
Dublin City University · IEUniversity of Rochester Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The generation of reactive oxygen species (ROS) and an imbalance of antioxidant defence mechanisms can result in oxidative stress. Several pro-atherogenic stimuli that promote intimal-medial thickening (IMT) and early arteriosclerotic disease progression share oxidative stress as a common regulatory pathway dictating vascular cell fate. The major source of ROS generated within the vascular system is the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes (Nox), of which seven members have been characterized. The Nox family are critical determinants of the redox state within the vessel wall that dictate, in part the pathophysiology of several vascular phenotypes. This review highlights the putative role of ROS in controlling vascular fate by promoting endothelial dysfunction, altering vascular smooth muscle phenotype and dictating resident vascular stem cell fate, all of which contribute to intimal medial thickening and vascular disease progression.

Indexed as

adventitial cellsarteriosclerotic diseaseendothelialintimal-medial thickeningNoxROSstem cellsvascular smooth muscle

Identifiers

PMID29135921
PMCPMC5745500
OpenAlexW2768682253

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.