Evidence map›Paper›PMID 31578516›Full record

ReviewNature reviews. Cardiology2020

Transcriptional and epigenetic regulation of macrophages in atherosclerosis.

Tatyana Kuznetsova, Koen H M Prange, Christopher K Glass, Menno P J de Winther

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed, 3 pooled it
14.0field-weighted citation impact, top 1% 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

220 citing papers in PubMed, 3 syntheses or guidelines pooled it, 372 citations in OpenAlex.

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160 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 3 countries.

Tatyana Kuznetsova *Experimental Vascular Biology, Department of Medical Biochemistry, Amsterdam University Medical Centers - location AMC, University of Amsterdam, Amsterdam, Netherlands.ORCID http://orcid.org/0000-0001-7533-3334
Koen H M Prange *Experimental Vascular Biology, Department of Medical Biochemistry, Amsterdam University Medical Centers - location AMC, University of Amsterdam, Amsterdam, Netherlands.ORCID http://orcid.org/0000-0002-9835-1735
Christopher K GlassDepartment of Cellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA, USA.
Menno P J de WintherExperimental Vascular Biology, Department of Medical Biochemistry, Amsterdam University Medical Centers - location AMC, University of Amsterdam, Amsterdam, Netherlands. m.dewinther@amsterdamumc.nl.ORCID http://orcid.org/0000-0002-4038-6636
Amsterdam University Medical Centers · NLUniversity of California San Diego · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Transcriptional GenomicsP01HL088093 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WITZTUM, JOSEPH L. · 2008 to 2018
$26.4M
Transcriptional co-regulators and macrophage gene expressionR01DK091183 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2011 to 2025
$9.9M
NHLBI NIH HHS P01 HL088093NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK091183
6 · The paper itself

Abstract

Monocytes and macrophages provide defence against pathogens and danger signals. These cells respond to stimulation in a fast and stimulus-specific manner by utilizing complex cascaded activation by lineage-determining and signal-dependent transcription factors. The complexity of the functional response is determined by interactions between triggered transcription factors and depends on the microenvironment and interdependent signalling cascades. Dysregulation of macrophage phenotypes is a major driver of various diseases such as atherosclerosis, rheumatoid arthritis and type 2 diabetes mellitus. Furthermore, exposure of monocytes, which are macrophage precursor cells, to certain stimuli can lead to a hypo-inflammatory tolerized phenotype or a hyper-inflammatory trained phenotype in a macrophage. In atherosclerosis, macrophages and monocytes are exposed to inflammatory cytokines, oxidized lipids, cholesterol crystals and other factors. All these stimuli induce not only a specific transcriptional response but also interact extensively, leading to transcriptional and epigenetic heterogeneity of macrophages in atherosclerotic plaques. Targeting the epigenetic landscape of plaque macrophages can be a powerful therapeutic tool to modulate pro-atherogenic phenotypes and reduce the rate of plaque formation. In this Review, we discuss the emerging role of transcription factors and epigenetic remodelling in macrophages in the context of atherosclerosis and inflammation, and provide a comprehensive overview of epigenetic enzymes and transcription factors that are involved in macrophage activation.

Indexed as

AtherosclerosisEpigenesis, GeneticMacrophage ActivationMacrophagesTranscription, Genetic

Identifiers

PMID31578516
PMCPMC7770754
OpenAlexW2977754107

What OpenQuestion holds

Textmetadata
LicenceTDM
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.