Evidence map›Paper›PMID 42848422›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

Transcriptional regulation and function of GPR18 in macrophage subtype specification.

Hebe Agustina Mena, Andreas Patsalos, Jake Altomare, Filippa Davidsson, Gergely Nagy, Wilhelm K Berger, Blenda Wong, Allison Rahtes, Gabrielle Fredman, Laszlo Nagy and 1 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Hebe Agustina Mena *Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Andreas Patsalos *Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-9022-4985
Jake AltomareCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0009-0007-4332-5242
Filippa DavidssonCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Gergely NagyDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Wilhelm K BergerDepartment of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0003-0727-7064
Blenda WongCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Allison RahtesDepartment of Molecular and Cellular Immunology, Albany Medical College, Albany, NY 12208.
Gabrielle FredmanDepartment of Molecular and Cellular Immunology, Albany Medical College, Albany, NY 12208.
Laszlo NagyDepartment of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0001-6653-2155
Matthew SpiteCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-8868-3648

Funding

Role of Inflammation-Resolving Lipid Mediators In Ischemic RevascularizationR01HL106173 · NHLBI · UNIVERSITY OF LOUISVILLE · PI SPITE, MATTHEW R · 2011 to 2023
$5.7M
DHA-derived resolvin production andsignaling in tissue repair macrophages in metabolic diseaseR01DK124782 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI NAGY, LASZLO, SPITE, MATTHEW R · 2020 to 2023
$2.3M
HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL106173HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK124782NHLBI NIH HHS R01 HL106173NIDDK NIH HHS R01 DK124782
6 · The paper itself

Abstract

Resolution of inflammation is mediated in part by agonists that engage immune cells to dampen inflammatory signaling, promote phagocytic functions, and facilitate tissue repair. G protein-coupled receptor 18 (GPR18) has emerged as an important proresolving receptor that is activated by endogenous mediators including Resolvin D2. However, very little is known about how GPR18 expression is controlled in immune cells, and its cell-autonomous roles during resolution of inflammation remain of interest. Here, we elucidated transcriptional and epigenetic regulation of

Indexed as

Gene Expression RegulationMacrophagesReceptors, G-Protein-CoupledTranscription, GeneticAnimalsCore Binding Factor Alpha 2 SubunitInflammationInterferon-gammaInterferon Regulatory Factor-8Interferon Regulatory FactorsMiceMice, Inbred C57BLNF-kappa BProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Signal TransductionCore Binding Factor Alpha 2 SubunitInterferon-gammaInterferon Regulatory Factor-8Interferon Regulatory FactorsNF-kappa BProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptors, G-Protein-CoupledRunx1 protein, mouseTrans-ActivatorsTranscription FactorsG protein–coupled receptorsmacrophagesresolution of inflammation

Identifiers

PMID42848422
PMCPMC13660429

What OpenQuestion holds

Textmetadata
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.