Evidence map›Paper›PMID 37003185›Full record

ReviewInternational immunopharmacology2023

Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.

Keqiang Chen, Wanghua Gong, Jiaqiang Huang, Teizo Yoshimura, Ji Ming Wang

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
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

5 authors at 3 institutions in 2 countries.

Keqiang ChenLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA. Electronic address: chenkeq@mail.nih.gov.
Wanghua GongBasic Research Program, Leidos Biomedical Research, Inc., Frederick, MD, USA.
Jiaqiang HuangLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA; College of Life Sciences, Beijing Jiaotong University, Beijing, PR China.
Teizo YoshimuraLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA.
Ji Ming WangLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA.
Frederick National Laboratory for Cancer Research · USBeijing Jiaotong University · CNLeidos (United States) · US

Funding

Role of Formylpeptide Receptors in Host DefenseZ01BC010725 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 2006 to 2008
$624k
Intramural NIH HHS Z01 BC010725NCI NIH HHS HHSN261201500003CNCI NIH HHS HHSN261201500003I
6 · The paper itself

Abstract

Formyl peptide receptor 2 (FPR2) and its mouse counterpart Fpr2 are the members of the G protein-coupled receptor (GPCR) family. FPR2 is the only member of the FPRs that interacts with ligands from different sources. FPR2 is expressed in myeloid cells as well as epithelial cells, endothelial cells, neurons, and hepatocytes. During the past years, some unusual properties of FPR2 have attracted intense attention because FPR2 appears to possess dual functions by activating or inhibiting intracellular signal pathways based on the nature, concentration of the ligands, and the temporal and spatial settings of the microenvironment in vivo, the cell types it interacts with. Therefore, FPR2 controls an abundant array of developmental and homeostatic signaling cascades, in addition to its "classical" capacity to mediate the migration of hematopoietic and non-hematopoietic cells including malignant cells. In this review, we summarize recent development in FPR2 research, particularly in its role in diseases, therefore helping to establish FPR2 as a potential target for therapeutic intervention.

Indexed as

Endothelial CellsReceptors, Formyl PeptideAnimalsMiceReceptors, LipoxinSignal TransductionReceptors, Formyl PeptideReceptors, LipoxinAnti-inflammationCrosstalkFPR2, LigandsHomeostasisMacrophage polarityPro-inflammation

Identifiers

PMID37003185
PMCPMC10149111
OpenAlexW4361245910

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.