Evidence map›Paper›PMID 30283459›Full record

ArticleFrontiers in immunology2018

Genome-Wide Inhibition of Pro-atherogenic Gene Expression by Multi-STAT Targeting Compounds as a Novel Treatment Strategy of CVDs.

Martyna Plens-Galaska, Malgorzata Szelag, Aida Collado, Patrice Marques, Susana Vallejo, Mariella Ramos-González, Joanna Wesoly, María Jesus Sanz, Concepción Peiró, Hans A R Bluyssen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

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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

10 authors at 4 institutions in 2 countries.

Martyna Plens-GalaskaDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University, Poznan, Poland.
Malgorzata SzelagDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University, Poznan, Poland.
Aida ColladoDepartment of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain.
Patrice MarquesDepartment of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain.
Susana VallejoDepartment of Pharmacology, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain.
Mariella Ramos-GonzálezDepartment of Pharmacology, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain.
Joanna WesolyLaboratory of High Throughput Technologies, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
María Jesus SanzDepartment of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain.
Concepción PeiróDepartment of Pharmacology, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain.
Hans A R BluyssenDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University, Poznan, Poland.
Adam Mickiewicz University in Poznań · PLINCLIVA Health Research Institute · ESHospital Universitario La Paz · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases (CVDs), including atherosclerosis, are globally the leading cause of death. Key factors contributing to onset and progression of atherosclerosis include the pro-inflammatory cytokines Interferon (IFN)α and IFNγ and the Pattern Recognition Receptor (PRR) Toll-like receptor 4 (TLR4). Together, they trigger activation of Signal Transducer and Activator of Transcription (STAT)s. Searches for compounds targeting the pTyr-SH2 interaction area of STAT3, yielded many small molecules, including STATTIC and STX-0119. However, many of these inhibitors do not seem STAT3-specific. We hypothesized that multi-STAT-inhibitors that simultaneously block STAT1, STAT2, and STAT3 activity and pro-inflammatory target gene expression may be a promising strategy to treat CVDs. Using comparative

Indexed as

AnimalsAtherosclerosisCardiovascular DiseasesCell LineCells, CulturedCyclic S-OxidesGene ExpressionGene Expression ProfilingGenome-Wide Association StudyHumansMaleMice, Inbred C57BLOxadiazolesQuinolinesSignal TransductionSmall Molecule LibrariesCyclic S-OxidesOxadiazolesQuinolinesSmall Molecule LibrariesstatticSTAT Transcription FactorsSTX-0119CVDs treatment strategyin silico dockingmulti-STAT inhibitorsSTATvascular inflammation

Identifiers

PMID30283459
PMCPMC6156247
OpenAlexW2891104624

What OpenQuestion holds

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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.