ArticleJACC. Basic to translational science2021
Selective FPR2 Agonism Promotes a Proresolution Macrophage Phenotype and Improves Cardiac Structure-Function Post Myocardial Infarction.
Article in JACC. Basic to translational science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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.
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.
Who cites it
31 citing papers in PubMed.
- Remote electroacupuncture conditioning protects the heart via fine-tuning the dual role of the SDF-1α/CXCR4 axis in myocardial ischemia-reperfusion injury.Chinese medicine · 2026Article
- Splenic erythrophagocytosis is regulated by ALX/FPR2 signaling.Haematologica · 2026Article
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.Journal of advanced research · 2026Review
- Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Investigation into ligand selectivity and bias at the formyl peptide receptor family.The Journal of pharmacology and experimental therapeutics · 2026Article
- Macrophage plasticity and metabolic control in muscle repair and disease.Frontiers in immunology · 2026Review
- Neutrophil death pathways in myocardial infarction: the balance between injury and repair.Frontiers in immunology · 2026Review
- Macrophage ITGAV is dispensable for post-infarction remodeling in mice and does not mediate fibronectin responses.Communications biology · 2025Article
- Involvement of formyl peptide receptor 2 in canine coronavirus infection: in vitro and in Silico approaches.Virology journal · 2025Article
- Resolution Pharmacology: State-of-the-art and therapeutic landscape.Pharmacological reviews · 2025Review
- FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy.Cell death & disease · 2025Article
- The roles of neutrophils in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Discovery and Optimization of Aryl Piperidinone Ureas as Selective Formyl Peptide Receptor 2 Agonists.ACS medicinal chemistry letters · 2024Article
- Structural basis of G protein-Coupled receptor CMKLR1 activation and signaling induced by a chemerin-derived agonist.PLoS biology · 2023Article
- Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis.Nature communications · 2023Article
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction.Cellular & molecular biology letters · 2023Review
- Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated inflammation following myocardial infarction (MI) leads to maladaptive healing and remodeling. The study characterized and evaluated a selective formyl peptide receptor 2 (FPR2) agonist BMS-986235 in cellular assays and in rodents undergoing MI. BMS-986235 activated G proteins and promoted β-arrestin recruitment, enhanced phagocytosis and neutrophil apoptosis, regulated chemotaxis, and stimulated interleukin-10 and monocyte chemoattractant protein-1 gene expression. Treatment with BMS-986235 improved mouse survival, reduced left ventricular area, reduced scar area, and preserved wall thickness. Treatment increased macrophage arginase-1 messenger RNA and CD206 receptor levels indicating a proresolution phenotype. In rats following MI, BMS-986235 preserved viable myocardium, attenuated left ventricular remodeling, and increased ejection fraction relative to control animals. Therefore, FPR2 agonism improves post-MI healing, limits remodeling and preserves function, and may offer an innovative therapeutic option to improve outcomes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.