Evidence map›Paper›PMID 30343819›Full record

ReviewAtherosclerosis2019

Nature and nurture of tissue-specific macrophage phenotypes.

Marten A Hoeksema, Christopher K Glass

Open access · greenAbstract readReview
In one paragraph

Review in Atherosclerosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

  1. Tissue signatures of human macrophages during homeostasis and activation.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  2. Article
  3. Article
  4. Macrophage Development and Function.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Monocyte/Macrophage Heterogeneity during Skin Wound Healing in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  11. Article
  12. Article
  13. Synovial inflammation in osteoarthritis progression.Nature reviews. Rheumatology · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Marten A HoeksemaDepartment of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
Christopher K GlassDepartment of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA; Department of Medicine, University of California San Diego, La Jolla, CA, USA. Electronic address: ckg@ucsd.edu.
University 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
SYNTHETIC SYSTEMSP50GM085764 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HASTY, JEFF M, IDEKER, TREY · 2010 to 2018
$23.3M
NHLBI NIH HHS P01 HL088093NIDDK NIH HHS P30 DK063491NIGMS NIH HHS P50 GM085764
6 · The paper itself

Abstract

Macrophages are key players in immunity and tissue homeostasis but can also contribute to a diverse range of human diseases, including cardiovascular diseases. Enhancers, cis-acting DNA elements regulating gene activity, have been shown to be crucial for control of macrophage development and function. The selection and activities of macrophage-specific enhancers are regulated by the combined actions of lineage determining transcription factors (LDTFs) and signal dependent transcription factors (SDTFs) that are specified by developmental origin and tissue-specific signals. As a consequence, each tissue resident macrophage population adopts a distinct phenotype. In this review, we discuss recent work on how environmental factors affect the activation status of enhancers and can lead to long-lasting epigenetic changes resulting in innate immune memory. Furthermore, we discuss how non-coding genetic variation affects gene expression by altering transcription factor binding through local and domain-wide mechanisms. These findings have implications for interpretation of non-coding risk alleles that are associated with human disease and efforts to target macrophages for therapeutic purposes.

Indexed as

Cellular MicroenvironmentEpigenesis, GeneticGene-Environment InteractionAnimalsCell PlasticityHumansImmunity, InnateImmunologic MemoryMacrophage ActivationMacrophagesSignal TransductionTranscription, GeneticEnhancerGenetic variationMacrophageTissue environment

Identifiers

PMID30343819
PMCPMC6399046
OpenAlexW2895336643

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.