Evidence map›Paper›PMID 27462873›Full record

ArticleeLife2016

Tissue damage drives co-localization of NF-κB, Smad3, and Nrf2 to direct Rev-erb sensitive wound repair in mouse macrophages.

Dawn Z Eichenfield, Ty Dale Troutman, Verena M Link, Michael T Lam, Han Cho, David Gosselin, Nathanael J Spann, Hanna P Lesch, Jenhan Tao, Jun Muto and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.0field-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

50 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Regulation of macrophage transcriptional dynamics during acute and chronic wound repair.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  4. Article
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  7. Reprogramming of the LXRα Transcriptome Sustains Macrophage Secondary Inflammatory Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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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

13 authors at 2 institutions in 2 countries.

Dawn Z EichenfieldDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.ORCID 0000-0002-1511-3804
Ty Dale TroutmanDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.ORCID 0000-0001-8925-8080
Verena M LinkDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.ORCID 0000-0002-3207-312X
Michael T LamDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.
Han ChoSalk Institute for Biological Sciences, La Jolla, United States.
David GosselinDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.
Nathanael J SpannDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.
Hanna P LeschDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.
Jenhan TaoDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.
Jun MutoDepartment of Dermatology, University of California, San Diego, San Diego, United States.
Richard L GalloDepartment of Dermatology, University of California, San Diego, San Diego, United States.
Ronald M EvansSalk Institute for Biological Sciences, La Jolla, United States.
Christopher K GlassDepartment of Cellular and Molecular Medicine, University of California, San Diego, San Diego, United States.ORCID 0000-0003-4344-3592
University of California San Diego · USSalk Institute for Biological Studies · US

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007198 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C, INSEL, PAUL A · 1985 to 2024
$29.3M
SYNTHETIC SYSTEMSP50GM085764 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HASTY, JEFF M, IDEKER, TREY · 2010 to 2018
$23.3M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
Contemporary Approaches to Cancer Cell Signaling and CommunicationT32CA009523 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DONOGHUE, DANIEL J, YANG, JING · 1985 to 2025
$12.1M
Transcriptional co-regulators and macrophage gene expressionR01DK091183 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2011 to 2025
$9.9M
Enhancer TherapyR01CA173903 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2012 to 2016
$6.3M
Spatial Regulation of Developmental Gene ExpressionR01HL105278 · NHLBI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2011 to 2019
$4.0M
NCI NIH HHS R01 CA173903NCI NIH HHS T32 CA009523NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK091183NIGMS NIH HHS P50 GM085764NIGMS NIH HHS T32 GM007198
6 · The paper itself

Abstract

Although macrophages can be polarized to distinct phenotypes in vitro with individual ligands, in vivo they encounter multiple signals that control their varied functions in homeostasis, immunity, and disease. Here, we identify roles of Rev-erb nuclear receptors in regulating responses of mouse macrophages to complex tissue damage signals and wound repair. Rather than reinforcing a specific program of macrophage polarization, Rev-erbs repress subsets of genes that are activated by TLR ligands, IL4, TGFβ, and damage-associated molecular patterns (DAMPS). Unexpectedly, a complex damage signal promotes co-localization of NF-κB, Smad3, and Nrf2 at Rev-erb-sensitive enhancers and drives expression of genes characteristic of multiple polarization states in the same cells. Rev-erb-sensitive enhancers thereby integrate multiple damage-activated signaling pathways to promote a wound repair phenotype.

Indexed as

Wound HealingAnimalsMacrophagesMiceNF-E2-Related Factor 2NF-kappa B p50 SubunitNuclear Receptor Subfamily 1, Group D, Member 1Receptors, Cytoplasmic and NuclearRepressor ProteinsSignal TransductionSkinSmad3 ProteinNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa B p50 SubunitNfkb1 protein, mouseNr1d1 protein, mouseNr1d2 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1Receptors, Cytoplasmic and NuclearRepressor ProteinsSmad3 ProteinSmad3 protein, mousechromosomesenhancerepigeneticsgenesmacrophagemouseRev-erbwound healing

Identifiers

PMID27462873
PMCPMC4963201
OpenAlexW2501636192

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.