ReviewLife (Basel, Switzerland)2021
Regulation of Inflammation and Oxidative Stress by Formyl Peptide Receptors in Cardiovascular Disease Progression.
Review in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 43 citations in OpenAlex.
- RvD1/FPR2 attenuates cerebral ischemic injury through inhibiting inflammation and oxidative stress.Scientific reports · 2026Article
- Sex-Specific Associations Between Cadmium Exposure and Mortality Risk in Cardiovascular Disease Patients: A Cohort Study Integrating Molecular Mechanisms of Myocardial Dysfunction.Cardiovascular toxicology · 2026Article
- Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026Review
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- Protective Effects of Cyclosporin H Against Sepsis-Induced Acute Kidney Injury via Modulation of Fpr1 Signaling and Inhibiting Pyroptosis.Research and reports in urology · 2026Article
- Sequential exposure to histological chorioamnionitis and postnatal hyperoxia alters gene expression in cord blood monocytes.Frontiers in pediatrics · 2026Article
- Late-Onset Multiple Acyl-CoA Dehydrogenase Deficiency (MADD): Clinical Features, Diagnostic Challenges, and the Role of Oxidative Stress in Pathophysiology.Antioxidants (Basel, Switzerland) · 2025Article
- Cardiovascular Health in the Shadow of Diabetes and Metabolic Dysfunction-Associated Steatotic Liver Disease: An Emerging Paradigm.Reviews in cardiovascular medicine · 2025Review
- Lipoxins as Modulators of Diseases.Cells · 2025Review
- Bioactive Compounds as Modulators of N-Formyl Peptide Signaling in Chronic Diseases.Molecules (Basel, Switzerland) · 2025Review
- Annexin-A1 deficiency uncovers female-specific pathways in blood pressure control and cardiovascular remodeling in mice.Communications biology · 2025Article
- Integrative multi-omics analysis of metabolic dysregulation induced by occupational benzene exposure in mice.The Science of the total environment · 2025Article
- Annexin A1: The dawn of ischemic stroke (Review).Molecular medicine reports · 2025Review
- Current Perspectives on the NF-κB Signaling Axis as a Potential Pharmacological Target in Cardiorenal Syndrome.Drug design, development and therapy · 2025Review
- Lipoxin ACardiovascular diabetology · 2024Article
- Turn-Adopting Peptidomimetic as a Formyl Peptide Receptor-1 Antagonist.ACS pharmacology & translational science · 2024Article
- Machine learning algorithms for predicting glioma patient prognosis based on CD163+FPR3+ macrophage signature.NPJ precision oncology · 2024Article
- Targeted Antioxidant Therapy Reduces Hyperglycemic Exacerbation of Myocardial Ischemia/Reperfusion Injury.The Journal of surgical research · 2024Article
- Transcriptome Study in Sicilian Patients with Autism Spectrum Disorder.Biomedicines · 2024Article
- Amniotic fluid stem cell-derived extracellular vesicles educate type 2 conventional dendritic cells to rescue autoimmune disorders in a multiple sclerosis mouse model.Journal of extracellular vesicles · 2024Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-coupled receptors (GPCRs) are the most important regulators of cardiac function and are commonly targeted for medical therapeutics. Formyl-Peptide Receptors (FPRs) are members of the GPCR superfamily and play an emerging role in cardiovascular pathologies. FPRs can modulate oxidative stress through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species (ROS) production whose dysregulation has been observed in different cardiovascular diseases. Therefore, many studies are focused on identifying molecular mechanisms of the regulation of ROS production. FPR1, FPR2 and FPR3 belong to the FPRs family and their stimulation triggers phosphorylation of intracellular signaling molecules and nonsignaling proteins that are required for NADPH oxidase activation. Some FPR agonists trigger inflammatory processes, while other ligands activate proresolving or anti-inflammatory pathways, depending on the nature of the ligands. In general, bacterial and mitochondrial formylated peptides activate a proinflammatory cell response through FPR1, while Annexin A1 and Lipoxin A4 are anti-inflammatory FPR2 ligands. FPR2 can also trigger a proinflammatory pathway and the switch between FPR2-mediated pro- and anti-inflammatory cell responses depends on conformational changes of the receptor upon ligand binding. Here we describe the detrimental or beneficial effects of the main FPR agonists and their potential role as new therapeutic and diagnostic targets in the progression of cardiovascular diseases.
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