AnxA1

Annexin A1 (AnxA1) is a glucocorticoid-regulated member of the annexin family that functions as a calcium-dependent phospholipid-binding protein and an endogenous mediator of inflammation resolution^[1][2]. Mechanistically, AnxA1 limits leukocyte recruitment, promotes neutrophil apoptosis, enhances macrophage-mediated clearance of apoptotic cells, and supports macrophage reprogramming toward a pro-resolving phenotype, thereby restoring tissue homeostasis after inflammatory responses^[1][3]. Through signaling mediated by formyl peptide receptors (FPRs), particularly FPR2/ALX, AnxA1 and its N-terminal peptide derivatives regulate inflammatory cell behavior and coordinate resolution-associated pathways^[1][4]. In disease models, AnxA1 contributes to mucosal repair by activating epithelial FPR-dependent signaling and NOX1-mediated redox pathways that promote epithelial migration and wound closure^[4]. Dysregulated AnxA1 expression has also been associated with cancer progression, inflammatory disorders, and viral infections, highlighting its context-dependent roles in disease pathophysiology^[2][5][6]. Compared with other annexin family members, AnxA1 is distinguished by its well-characterized pro-resolving and immunoregulatory functions, whereas related isoforms often display broader roles in membrane dynamics, stress responses, or regulated cell death pathways^[2][7]. For experimental applications, the AnxA1-derived peptide Ac2-26 reproduces key biological activities of the full-length protein through FPR signaling and is widely used as a pharmacological tool to investigate resolution biology, tissue repair, and anti-inflammatory mechanisms^[4][6].

References: