Evidence map›Paper›PMID 31909300›Full record

ArticleJACC. Basic to translational science2019

Preservation of Post-Infarction Cardiac Structure and Function via Long-Term Oral Formyl Peptide Receptor Agonist Treatment.

Ricardo A García, Bruce R Ito, John A Lupisella, Nancy A Carson, Mei-Yin Hsu, Gayani Fernando, Madeleine Heroux, Michel Bouvier, Elizabeth Dierks, Ellen K Kick and 13 more

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Review
  3. Investigation into ligand selectivity and bias at the formyl peptide receptor family.The Journal of pharmacology and experimental therapeutics · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. TheFrontiers in immunology · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Molecular Pharmacology of Inflammation Resolution in Atherosclerosis.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Annexin A1 attenuates cardiac diastolic dysfunction in mice with inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 5 institutions in 3 countries.

Ricardo A GarcíaDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Bruce R ItoDepartment of Medicine, University of California San Diego, San Diego, California.
John A LupisellaDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Nancy A CarsonDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Mei-Yin HsuDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Gayani FernandoDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Madeleine HerouxInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec, Canada.
Michel BouvierInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec, Canada.
Elizabeth DierksDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Ellen K KickDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
David A GordonDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Jian ChenDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Gabe MintierDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Marilyn CarrierInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec, Canada.
Stéphane St-OngeInstitute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec, Canada.
Himanshu ShahDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Jordan TowneDepartment of Medicine, University of California San Diego, San Diego, California.
Marcela Sotelo BucardoDepartment of Medicine, University of California San Diego, San Diego, California.
Xiuying MaDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Carol S RyanDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Nicholas R WurtzDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Jacek OstrowskiDepartment of Cardiovascular and Fibrosis Drug Discovery, Bristol-Myers Squibb Company, Pennington, New Jersey.
Francisco J VillarrealDepartment of Medicine, University of California San Diego, San Diego, California.
Bristol-Myers Squibb (Germany) · DEBristol-Myers Squibb (United States) · USUniversity of California, San Diego · USUniversité de Montréal · CAInstitute for Research in Immunology and Cancer · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated inflammation following myocardial infarction (MI) promotes left ventricular (LV) remodeling and loss of function. Targeting inflammation resolution by activating formyl peptide receptors (FPRs) may limit adverse remodeling and progression towards heart failure. This study characterized the cellular and signaling properties of Compound 43 (Cmpd43), a dual FPR1/FPR2 agonist, and examined whether Cmpd43 treatment improves LV and infarct remodeling in rodent MI models. Cmpd43 stimulated FPR1/2-mediated signaling, enhanced proresolution cellular function, and modulated cytokines. Cmpd43 increased LV function and reduced chamber remodeling while increasing proresolution macrophage markers. The findings demonstrate that FPR agonism improves cardiac structure and function post-MI.

Indexed as

agonistCmpd43, Compound 43Compound 43formyl peptide receptorFPR, formyl peptide receptorheart failureHF, heart failureIL, interleukinIR, ischemia–reperfusionKO, knockoutLAD, left anterior descendingLV, left ventricularMI, myocardial infarctionmyocardial infarctionPV, pressure–volumeSAA, serum amyloid AWT, wild-type

Identifiers

PMID31909300
PMCPMC6939031
OpenAlexW2983278329

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.