Formyl peptide and its receptor system as a novel target for the prevention and treatment of neuroinflammation-related diseases

Neuroinflammation is a hallmark pathological feature of various central nervous system (CNS) disorders. Persistent activation can trigger an imbalance between pro- and anti-inflammatory homeostasis, thereby exacerbating neuronal injury, demyelination, and blood-brain barrier (BBB) disruption, ultimately leading to irreversible loss of neurological function. Formyl peptides and their receptors are critical drivers of neuroinflammation. As members of the G protein-coupled receptor (GPCR) family, formyl peptide receptors (FPRs) primarily recognize exogenous bacterial formyl peptides and endogenous damage-associated peptides, thereby modulating pathophysiological processes such as immune cell chemotaxis, inflammatory cytokine release, and tissue repair. Recent studies have demonstrated that FPRs are functionally expressed in microglia, astrocytes, and neurons of the CNS. Aberrant activation or silencing of FPRs is closely linked to the initiation, maintenance, and resolution of neuroinflammation and plays a pivotal role in neuroinflammation-related diseases. This review focuses on the mechanisms by which the formyl peptide/receptor system mediates neuroinflammation in neural cells. Furthermore, we propose potential therapeutic strategies targeting FPRs to modulate neuroinflammation and provide new perspectives for the prevention and treatment of neuroinflammation-related disorders.