Evidence map›Paper›PMID 21697732›Full record

ReviewJournal of cardiovascular pharmacology2012

Anti-inflammation therapy by activation of prostaglandin EP4 receptor in cardiovascular and other inflammatory diseases.

Eva H C Tang, Peter Libby, Paul M Vanhoutte, Aimin Xu

Abstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.3field-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

48 citing papers in PubMed, 81 citations in OpenAlex.

  1. Trial
  2. Genetic variation in the prostaglandin E2 pathway is associated with primary graft dysfunction.American journal of respiratory and critical care medicine · 2014
    Trial
  3. Article
  4. Review
  5. Article
  6. Linking Lipid Metabolism and Immune Function: New Insights into Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  7. Investigating the role of the mPGES-PGE₂-EP4 pathway inFrontiers in veterinary science · 2025
    Article
  8. SPMs exert anti-inflammatory and pro-resolving effects through positive allosteric modulation of the prostaglandin EP4 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
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  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

4 authors at 2 institutions in 2 countries.

Eva H C TangDepartment of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong. evatang1@hku.hk
Peter Libby
Paul M Vanhoutte
Aimin Xu
University of Hong Kong · HKHarvard University · US

Funding

Molecular Determinants of Arterial Remodeling in AtherogenesisR01HL080472 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2005 to 2018
$5.0M
Inflammatory Mechanisms of AtherosclerosisR01HL034636 · NHLBI · TUFTS UNIVERSITY BOSTON · PI LIBBY, PETER · 1985 to 2006
$1.9M
CONTROL OF GROWTH OF VASCULAR WALL CELLSR37HL034636 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 1993 to 2002
$1.2M
NHLBI NIH HHS HL-34636NHLBI NIH HHS HL-80472NHLBI NIH HHS R01 HL034636NHLBI NIH HHS R01 HL080472NHLBI NIH HHS R37 HL034636
6 · The paper itself

Abstract

Prostaglandin E2 constitutes a major cyclooxygenase-2-derived prostanoid produced at inflammatory sites. In vitro and in vivo data support its role as a modulator of inflammation. Prostaglandin E2 exerts anti-inflammatory effects by binding to one of its receptors, the prostaglandin E receptor 4 (EP4), thereby modulating macrophage and T lymphocyte functions that participate crucially in innate and adaptive immunity and tissue remodeling and repair. The activation of EP4 suppresses the release of cytokines and chemokines from macrophages and T cells, inhibits the proliferation and the activation of T cells, and induces T-cell apoptosis. Lack of EP4 in bone marrow-derived cells accelerates local inflammation in atherosclerotic and aneurysm lesions and increases the prevalence of aneurysm formation. An EP4 agonist promotes graft survival in allograft cardiac transplantation and dampens tissue damage after myocardial ischemia. Anti-inflammatory actions of EP4 agonism may benefit other inflammatory disorders, including colitis and gastric ulcers. By contrast, EP4 acts as a proinflammatory mediator in encephalomyelitis, skin inflammation, and arthritis by promoting T helper (Th) 1 differentiation and Th17 expansion. Overall, EP4 activation produces powerful anti-inflammatory responses in many experimental diseases, rendering EP4 agonists attractive agents to attenuate syndromes associated with inflammation.

Indexed as

AnimalsAnti-Inflammatory AgentsApoptosisCardiovascular DiseasesCyclooxygenase 2DinoprostoneHumansInflammationInflammation MediatorsMacrophagesReceptors, Prostaglandin E, EP4 SubtypeT-LymphocytesAnti-Inflammatory AgentsCyclooxygenase 2DinoprostoneInflammation MediatorsReceptors, Prostaglandin E, EP4 Subtype

Identifiers

PMID21697732
PMCPMC3191244
OpenAlexW2090662878

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.