title: Leukocyte chemoattractant receptor FPR2 may accelerate atherogenesis.
abstract: Atherosclerosis is a chronic inflammatory disease and the number one cause of mortality worldwide. The fundamental causes of atherosclerosis have not been precisely delineated, although pathogenesis clearly involves endothelial dysfunction and both innate and adaptive immunity. Recent evidence suggests that formyl peptide receptor 2 (FPR2), a G protein-coupled receptor (GPCR), mediates a range of inflammatory responses including superoxide production in neutrophils, chemotaxis of monocytes and neutrophils, CCL2 production in endothelial cells (ECs) and monocytes, and increased CXCL8 expression in neutrophils, which are all related with atherogenesis. Therefore, we propose that FPR2 may play a pathogenic role in atherogenesis.
authors.affiliation: Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States. wanwu@niaid.nih.gov
authors.forename: Wuzhou
authors.initials: W
authors.lastname: Wan
authors.forename: Ji-Liang
authors.initials: JL
authors.lastname: Gao
mesh_terms: D050197:Atherosclerosis / Q000503:physiopathology*; D006801:Humans; D007962:Leukocytes / Q000502:physiology*; D009000:Monocytes / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D044042:Receptors, Formyl Peptide / Q000502:physiology*; D044067:Receptors, Lipoxin / Q000502:physiology*; D013481:Superoxides / Q000378:metabolism
chemical_list: C105101:FPR2 protein, human; D044042:Receptors, Formyl Peptide; D044067:Receptors, Lipoxin; D013481:Superoxides