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Review
. 2025 Jun;77(3):593-609.
doi: 10.1007/s43440-025-00704-x. Epub 2025 Mar 18.

Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases

Affiliations
Review

Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases

Jiaying Wang et al. Pharmacol Rep. 2025 Jun.

Abstract

Formyl peptide receptor 2 (FPR2) is a G protein-coupled receptor with seven transmembrane domains, widely distributed in human cells. It plays a crucial role in inflammation-related diseases. Known for its "double-edged sword" nature, FPR2 can bind a variety of exogenous and endogenous ligands, mediating both pro-inflammatory and anti-inflammatory responses in tissues such as eyes, liver, joints, lungs, nerves, and blood vessels. FPR2's bioactivities are regulated by a complex network of genes and signaling pathways. However, the precise regulatory mechanisms governing its functions in different inflammatory conditions are still not well understood. This review summarizes the FPR2's activities in various inflammation-related diseases and looks into its potential as a therapeutic target. This review highlights recent advances in developing exogenous agonists for FPR2 and discusses receptor expression across species to support nonclinical research. Overall, this review aims to clarify FPR2's role in inflammation and provide insights for the development of new drugs against inflammatory diseases.

Keywords: Endogenous ligands; Exogenous agonists; Formyl peptide receptor 2; Inflammatory diseases; Therapeutic potential.

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Conflict of interest statement

Declarations. Conflict of interest: The authors declare no competing interests.

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References

    1. Chen L, Deng H, Cui H, Fang J, Zuo Z, Deng J, et al. Inflammatory responses and inflammation-associated diseases in organs. Oncotarget. 2018;9:7204–18. - PubMed - DOI
    1. Murakami M, Hirano T. The molecular mechanisms of chronic inflammation development. Front Immunol. 2012;3:323. - PubMed - PMC - DOI
    1. Bernardette Martínez-Rizo A, Fosado-Rodríguez R, César Torres-Romero J, César Lara-Riegos J, Alberto Ramírez-Camacho M, Ly Arroyo Herrera A, et al. Models in vivo and in vitro for the study of acute and chronic inflammatory activity: a comprehensive review. Int Immunopharmacol. 2024;135:112292. - PubMed - DOI
    1. Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454:428–35. - PubMed - DOI
    1. Filep JG, Sekheri M, El Kebir D. Targeting formyl peptide receptors to facilitate the resolution of inflammation. Eur J Pharmacol. 2018;833:339–48. - PubMed - DOI

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