Evidence map›Paper›PMID 27166190›Full record

ReviewOncotarget2016

Targeted inhibition of STATs and IRFs as a potential treatment strategy in cardiovascular disease.

Malgorzata Szelag, Anna Piaszyk-Borychowska, Martyna Plens-Galaska, Joanna Wesoly, Hans A R Bluyssen

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  18. Type-I interferons in atherosclerosis.The Journal of experimental medicine · 2020
    Review
  19. Article
  20. Scrodentoids H and I, a Pair of Natural Epimerides fromEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
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

5 authors at 1 institution in 1 country.

Malgorzata SzelagDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
Anna Piaszyk-BorychowskaDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
Martyna Plens-GalaskaDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
Joanna WesolyLaboratory of High Throughput Technologies, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
Hans A R BluyssenDepartment of Human Molecular Genetics, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
Adam Mickiewicz University in Poznań · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Key factors contributing to early stages of atherosclerosis and plaque development include the pro-inflammatory cytokines Interferon (IFN)α, IFNγ and Interleukin (IL)-6 and Toll-like receptor 4 (TLR4) stimuli. Together, they trigger activation of Signal Transducer and Activator of Transcription (STAT) and Interferon Regulatory Factor (IRF) families. In particular, STAT1, 2 and 3; IRF1 and 8 have recently been recognized as prominent modulators of inflammation, especially in immune and vascular cells during atherosclerosis. Moreover, inflammation-mediated activation of these STATs and IRFs coordinates a platform for synergistic amplification leading to pro-atherogenic responses.Searches for STAT3-targeting compounds, exploring the pTyr-SH2 interaction area of STAT3, yielded many small molecules including natural products. Only a few inhibitors for other STATs, but none for IRFs, are described. Promising results for several STAT3 inhibitors in recent clinical trials predicts STAT3-inhibiting strategies may find their way to the clinic. However, many of these inhibitors do not seem STAT-specific, display toxicity and are not very potent. This illustrates the need for better models, and screening and validation tools for novel STAT and IRF inhibitors.This review presents a summary of these findings. It postulates STAT1, STAT2 and STAT3 and IRF1 and IRF8 as interesting therapeutic targets and targeted inhibition could be a potential treatment strategy in CVDs. In addition, it proposes a pipeline approach that combines comparative in silico docking of STAT-SH2 and IRF-DBD models with in vitro STAT and IRF activation inhibition validation, as a novel tool to screen multi-million compound libraries and identify specific inhibitors for STATs and IRFs.

Indexed as

Anticholesteremic AgentsAtherosclerosisClinical Trials as TopicDrug Evaluation, PreclinicalHumansInflammationInterferon-alphaInterferon-gammaInterferon Regulatory FactorsInterleukin-6Molecular Docking SimulationMolecular Targeted TherapyPhosphorylationPlaque, AtheroscleroticSignal TransductionSTAT Transcription FactorsAnticholesteremic AgentsIL6 protein, humanInterferon-alphaInterferon-gammaInterferon Regulatory FactorsInterleukin-6STAT Transcription FactorsTLR4 protein, humanToll-Like Receptor 4in silico modelingIRFSTATtherapeutic strategyvascular inflammation

Identifiers

PMID27166190
PMCPMC5217051
OpenAlexW2346417149

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.