Evidence map›Paper›PMID 29191809›Full record

ArticleJournal of the American Heart Association2017

Molecular Fingerprint for Terminal Abdominal Aortic Aneurysm Disease.

Gabor Gäbel, Bernd H Northoff, Irina Weinzierl, Stefan Ludwig, Irene Hinterseher, Wolfgang Wilfert, Daniel Teupser, Stefan A Doderer, Hendrik Bergert, Frank Schönleben and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.5field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020
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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 4 institutions in 2 countries.

Gabor GäbelDepartment of Vascular and Endovascular Surgery, Ludwig-Maximilians-University Munich, Munich, Germany gabor.gaebel@med.uni-muenchen.de.
Bernd H NorthoffInstitute of Laboratory Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.
Irina WeinzierlDepartment of Vascular and Endovascular Surgery, Ludwig-Maximilians-University Munich, Munich, Germany.
Stefan LudwigDepartment of Visceral, Thoracic and Vascular Surgery, University Hospital Carl Gustav Carus Technische Universität Dresden, Dresden, Germany.
Irene HinterseherDepartment of Visceral, Thoracic and Vascular Surgery, University Hospital Carl Gustav Carus Technische Universität Dresden, Dresden, Germany.
Wolfgang WilfertInstitute of Laboratory Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.
Daniel TeupserInstitute of Laboratory Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.
Stefan A DodererDepartment of Vascular Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Hendrik BergertDepartment of Visceral, Thoracic and Vascular Surgery, University Hospital Carl Gustav Carus Technische Universität Dresden, Dresden, Germany.
Frank SchönlebenDepartment of Vascular and Endovascular Surgery, Ludwig-Maximilians-University Munich, Munich, Germany.
Jan H N LindemanDepartment of Vascular Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Lesca M HoldtInstitute of Laboratory Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DEUniversity Hospital Carl Gustav Carus · DELeiden University Medical Center · NLTU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinical decision making in abdominal aortic aneurysms (AAA) relies completely on diameter. At this point, improved decision tools remain an unmet medical need. Our goal was to identify changes at the molecular level specifically leading up to AAA rupture. METHODS AND

resultsAortic wall tissue specimens were collected during open elective (eAAA; n=31) or emergency repair of ruptured AAA (rAAA; n=17), and gene expression was investigated using microarrays. Identified candidate genes were validated with quantitative real-time polymerase chain reaction in an independent sample set (eAAA: n=46; rAAA: n=18). Two gene sets were identified, 1 set containing 5 genes linked to terminal progression, that is, positively associated with progression of larger AAA, and with rupture (

conclusionsOur study shows a specific molecular fingerprint for terminal AAA disease. These changes appear to converge at activation of HIF-1α signaling in mesenchymal cells. Aspects of this cascade might represent targets for rupture risk assessment.

Indexed as

TranscriptomeAorta, AbdominalAortic Aneurysm, AbdominalAortic RuptureCells, CulturedFibroblastsGene Expression ProfilingGene Regulatory NetworksGenetic Association StudiesGenetic MarkersHumansHypoxia-Inducible Factor 1, alpha SubunitOligonucleotide Array Sequence AnalysisPredictive Value of TestsReal-Time Polymerase Chain ReactionRisk FactorsGenetic MarkersHIF1A protein, humanHypoxia-Inducible Factor 1, alpha Subunitabdominal aortic aneurysmangiogenesisendothelial cell differentiationgene microarrayhypoxia‐inducible factor 1

Identifiers

PMID29191809
PMCPMC5779007
OpenAlexW2773188710

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.