No evidence for the involvement of the lipoxin A4 receptor (FPR2/ALX) gene in the susceptibility to coronary artery disease

摘要

The lipoxin A4 receptor (FPR2/ALX) belongs to the class A rhodopsin G protein-coupled receptor superfamily and plays a role in chemotaxis and activation of phagocytes (1). Several structurally diverse agonistic ligands, including peptides and lipid mediators have been shown to bind to the FPR2/ALX (2). Since the discovery of serum amyloid A (SAA) as a pro-inflammatory ligand for FPR2/ALX, more peptides were identified, which all mediate a pro-inflammatory activation of leukocytes through FPR2/ALX (1). In contrast, FPR2/ALX can also bind anti-inflammatory ligands, such as lipoxin A4 (LXA4) and annexin-1 (2). Indeed, LXA4 was shown to inhibit neutrophil migration, to induce chemotaxis of mono-cytes and to promote the non-phlogistic phagocytosis of apoptotic neutrophils by macrophages (2). Thus, FPR2/ALX might induce anti-inflammatory effects when pro-resolving mediators are present.