Evidence map›Paper›PMID 30987671›Full record

ArticleArthritis research & therapy2019

Gene expression analysis of vascular pathophysiology related to anti-TNF treatment in rheumatoid arthritis.

Szilárd Póliska, Timea Besenyei, Edit Végh, Attila Hamar, Anita Pusztai, Andrea Váncsa, Nóra Bodnár, Szilvia Szamosi, Mária Csumita, György Kerekes and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Observational
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 at 2 institutions in 1 country.

Szilárd PóliskaDepartment of Biochemistry and Molecular Biology, University of Debrecen Faculty of Medicine, Debrecen, Hungary.
Timea BesenyeiDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Edit VéghDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Attila HamarDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Anita PusztaiDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Andrea VáncsaDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Nóra BodnárDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Szilvia SzamosiDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Mária CsumitaDepartment of Biochemistry and Molecular Biology, University of Debrecen Faculty of Medicine, Debrecen, Hungary.
György KerekesDepartment of Angiology, University of Debrecen Faculty of Medicine, Debrecen, Hungary.
Zoltán SzabóDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Zoltán NagyDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Gabriella SzűcsDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Sándor SzántóDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary.
Gábor ZahuczkyUD Genomed Ltd., Debrecen, Hungary.
László NagyDepartment of Biochemistry and Molecular Biology, University of Debrecen Faculty of Medicine, Debrecen, Hungary.
Zoltán SzekaneczDepartment of Rheumatology, University of Debrecen Faculty of Medicine, Nagyerdei str 98, Debrecen, 4032, Hungary. szekanecz.zoltan@med.unideb.hu.
University of Debrecen · HUUD-GenoMed (Hungary) · HU

Funding

PPARgamma as an architectural regulator of gene expression in endocrine signalingR01DK115924 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI NAGY, LASZLO · 2018 to 2021
$1.6M
European Union GINOP-2.3.2-15-2016-00015European Union GINOP-2.3.2-15-2016-00050European Union TAMOP-4.2.4.A/2-11/1-2012-0001
6 · The paper itself

Abstract

objectivesImpaired vascular pathophysiology and increased cardiovascular (CV) mortality are associated with rheumatoid arthritis (RA). To date, no genomic analysis of RA- and RA treatment-related vascular pathophysiology has been published. In this pilot study, we performed gene expression profiling in association with vascular pathophysiology in RA patients.

methodsSixteen and 19 biologic-naïve RA patients were included in study 1 and study 2, respectively. In study 1, genetic signatures determined by microarray were related to flow-mediated vasodilation (FMD), pulse-wave velocity (PWV), and common carotid intima-media thickness (IMT) of patients. In study 2, clinical response (cR) vs non-response (cNR) to 1-year etanercept (ETN) or certolizumab pegol (CZP) treatment, as well as "vascular" response (vR) vs non-response (vNR) to biologics, were also associated with genomic profiles. Multiple testing could not be performed due to the relatively small number of patients; therefore, our pilot study may lack power.

resultsIn study 1, multiple genes were up- or downregulated in patients with abnormal vs normal FMD, IMT, and PWV. In study 2, there were 13 cR and 6 cNR anti-tumor necrosis factor (TNF)-treated patients. In addition, 10, 9, and 8 patients were FMD-20%, IMT-20%, and PWV-20% responders. Again, vascular responder status was associated with changes of the expression of various genes. The highest number of genes showing significant enrichment were involved in positive regulation of immune effector process, regulation of glucose transport, and Golgi vesicle budding.

conclusionDifferential expression of multiple genetic profiles may be associated with vascular pathophysiology associated with RA. Moreover, distinct genetic signatures may also be associated with clinical and vascular responses to 1-year anti-TNF treatment.

Indexed as

AdultArthritis, RheumatoidCarotid Intima-Media ThicknessCertolizumab PegolEtanerceptFemaleGene Expression ProfilingGene Expression RegulationHumansMaleMiddle AgedPilot ProjectsPulse Wave AnalysisTumor Necrosis Factor-alphaVasodilationCertolizumab PegolEtanerceptTumor Necrosis Factor-alphaAtherosclerosisCertolizumab pegolEtanerceptGene expressionGenetic signaturePredictionResponseRheumatoid arthritisVascular pathology

Identifiers

PMID30987671
PMCPMC6466794
OpenAlexW2946430516

What Socratic 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 Socratic graph.