Evidence map›Paper›PMID 31821440›Full record

ReviewThe Journal of experimental medicine2020

Type-I interferons in atherosclerosis.

Hung-Jen Chen, Sander W Tas, Menno P J de Winther

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

  1. Pooled it
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  9. Research progress on macrophage regulation of atherosclerosis.Frontiers in cardiovascular medicine · 2026
    Review
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  20. The IRG1-itaconate axis protects from cholesterol-induced inflammation and atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

3 authors at 2 institutions in 2 countries.

Hung-Jen ChenExperimental Vascular Biology, Department of Medical Biochemistry, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.
Sander W TasAmsterdam Rheumatology and Immunology Center, Department of Rheumatology and Clinical Immunology, and Laboratory for Experimental Immunology, Academic Medical Center/University of Amsterdam, Amsterdam, Netherlands.
Menno P J de WintherExperimental Vascular Biology, Department of Medical Biochemistry, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.
Amsterdam University Medical Centers · NLAmsterdam UMC Location University of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of dyslipidemia and inflammation in atherosclerosis is well established. Along with effective lipid-lowering treatments, the recent success of clinical trials with anti-inflammatory therapies and the accelerated atherosclerosis in many autoimmune diseases suggest that targeting inflammation may open new avenues for the prevention and the treatment for cardiovascular diseases (CVDs). In the past decades, studies have widened the role of type-I interferons (IFNs) in disease, from antivirus defense to autoimmune responses and immuno-metabolic syndromes. While elevated type-I IFN level in serum is associated with CVD incidence in patients with interferonopathies, experimental data have attested that type-I IFNs affect plaque-residing macrophages, potentiate foam cell and extracellular trap formation, induce endothelial dysfunction, alter the phenotypes of dendritic cells and T and B lymphocytes, and lead to exacerbated atherosclerosis outcomes. In this review, we discuss the production and the effects of type-I IFNs in different atherosclerosis-associated cell types from molecular biology studies, animal models, and clinical observations, and the potential of new therapies against type-I IFN signaling for atherosclerosis.

Indexed as

AnimalsAtherosclerosisB-LymphocytesDendritic CellsHumansInflammationInterferon Type ISignal TransductionT-LymphocytesInterferon Type I

Identifiers

PMID31821440
PMCPMC7037237
OpenAlexW2992966803

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.