Evidence map›Paper›PMID 34699386›Full record

ArticleThe Journal of clinical investigation2021

The resolvin D1 receptor GPR32 transduces inflammation resolution and atheroprotection.

Hildur Arnardottir, Silke Thul, Sven-Christian Pawelzik, Glykeria Karadimou, Gonzalo Artiach, Alessandro L Gallina, Victoria Mysdotter, Miguel Carracedo, Laura Tarnawski, April S Caravaca and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Role of Inflammatory and Proresolving Mediators in Endothelial Dysfunction.Basic & clinical pharmacology & toxicology · 2025
    Review
  11. Review
  12. Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025
    Review
  13. Exploring G Protein-Coupled Receptors in Hematological Cancers.ACS pharmacology & translational science · 2024
    Article
  14. Review
  15. Review
  16. Review
  17. Biosynthesis of resolvin D1, resolvin D2, and RCTR1 from 7,8(S,S)-epoxytetraene in human neutrophils and macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Hildur ArnardottirDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Silke ThulDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Sven-Christian PawelzikDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Glykeria KaradimouDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Gonzalo ArtiachDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Alessandro L GallinaDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Victoria MysdotterDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Miguel CarracedoDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Laura TarnawskiDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
April S CaravacaDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Roland BaumgartnerDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Daniel Fj KetelhuthDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Peder S OlofssonDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Gabrielle Paulsson-BerneDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Göran K HanssonDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Magnus BäckDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine Solna, Karolinska Institute, and.
Karolinska Institutet · SEKarolinska University Hospital · SEUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is a hallmark of atherosclerosis and results from an imbalance between proinflammatory and proresolving signaling. The human GPR32 receptor, together with the ALX/FPR2 receptor, transduces biological actions of several proresolving mediators that stimulate resolution of inflammation. However, since no murine homologs of the human GPR32 receptor exist, comprehensive in vivo studies are lacking. Using human atherosclerotic lesions from carotid endarterectomies and creating a transgenic mouse model expressing human GPR32 on a Fpr2×ApoE double-KO background (hGPR32myc×Fpr2-/-×Apoe-/-), we investigated the role of GPR32 in atherosclerosis and self-limiting acute inflammation. GPR32 mRNA was reduced in human atherosclerotic lesions and correlated with the immune cell markers ARG1, NOS2, and FOXP3. Atherosclerotic lesions, necrotic core, and aortic inflammation were reduced in hGPR32mycTg×Fpr2-/-×Apoe-/- transgenic mice as compared with Fpr2-/-×Apoe-/- nontransgenic littermates. In a zymosan-induced peritonitis model, the hGPR32mycTg×Fpr2-/-×Apoe-/- transgenic mice had reduced inflammation at 4 hours and enhanced proresolving macrophage responses at 24 hours compared with nontransgenic littermates. The GPR32 agonist aspirin-triggered resolvin D1 (AT-RvD1) regulated leukocyte responses, including enhancing macrophage phagocytosis and intracellular signaling in hGPR32mycTg×Fpr2-/-×Apoe-/- transgenic mice, but not in Fpr2-/-×Apoe-/- nontransgenic littermates. Together, these results provide evidence that GPR32 regulates resolution of inflammation and is atheroprotective in vivo.

Indexed as

AtherosclerosisAnimalsDisease Models, AnimalDocosahexaenoic AcidsFemaleHumansInflammationMacrophagesMaleMiceMice, Knockout, ApoEPeritonitisPhagocytosisReceptors, G-Protein-CoupledSignal TransductionDocosahexaenoic AcidsGPR32 protein, humanReceptors, G-Protein-Coupledresolvin D1AtherosclerosisCardiologyG protein–coupled receptorsInflammation

Identifiers

PMID34699386
PMCPMC8670838
OpenAlexW3209613712

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.