Evidence map›Paper›PMID 34679682›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Patient Endothelial Colony-Forming Cells to Model Coronary Artery Disease Susceptibility and Unravel the Role of Dysregulated Mitochondrial Redox Signalling.

Marie Besnier, Meghan Finemore, Christine Yu, Katharine A Kott, Stephen T Vernon, Nicole A Seebacher, Elijah Genetzakis, Anamarija Furman, Owen Tang, Ryan L Davis and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

17 authors.

Marie BesnierCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Meghan FinemoreCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Christine YuCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Katharine A KottCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Stephen T VernonCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Nicole A SeebacherDepartment of Oncology, University of Oxford, Oxford OX1 2JD, UK.
Elijah GenetzakisCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Anamarija FurmanCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Owen TangCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Ryan L DavisNeurogenetics Group, Kolling Institute, St Leonards, NSW 2065, Australia.
Thomas HansenCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Peter J PsaltisSouth Australian Health and Medical Research Institute, Adelaide, SA 5000, Australia.
Kristen J BubbCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Steven G WiseSchool of Medical Sciences, Chronic Diseases Theme, University of Sydney, Sydngy, NSW 2006, Australia.ORCID 0000-0001-7964-819X
Stuart M GrieveFaculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia.
Belinda A Di BartoloCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.
Gemma A FigtreeCardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanisms involved in the individual susceptibility to atherosclerotic coronary artery disease (CAD) beyond traditional risk factors are poorly understood. Here, we describe the utility of cultured patient-derived endothelial colony-forming cells (ECFCs) in examining novel mechanisms of CAD susceptibility, particularly the role of dysregulated redox signalling. ECFCs were selectively cultured from peripheral blood mononuclear cells from 828 patients from the BioHEART-CT cohort, each with corresponding demographic, clinical and CT coronary angiographic imaging data. Spontaneous growth occurred in 178 (21.5%) patients and was more common in patients with hypertension (OR 1.45 (95% CI 1.03-2.02),

Indexed as

atherosclerosisbiomarkerscoronary artery diseaseendothelial cellsrisk factors

Identifiers

PMID34679682
PMCPMC8532880

What OpenQuestion holds

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Registered trials

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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.