Formyl peptide receptors in the microglial activation: New perspectives and therapeutic potential for neuroinflammation

Secondary neurological impairment mediated by neuroinflammation is recognized as a crucial pathological factor in central nervous system (CNS) diseases. Currently, there exists a lack of specific therapies targeting neuroinflammation. Given that microglia constitute the primary immune cells involved in the neuroinflammatory response, a thorough comprehension of their role in CNS diseases is imperative for the development of efficacious treatments. Recent investigations have unveiled the significance of formyl peptide receptors (FPRs) in various neuroinflammatory diseases associated with microglial overactivation. Consequently, FPRs emerge as promising targets for modulating the neuroinflammatory response. This review aims to comprehensively explore the therapeutic potential of targeting FPRs in the management of microglia‐mediated neuroinflammation. It delineates the molecular characteristics and functions of FPRs, elucidates their involvement in the inflammatory response linked to microglial overactivation, and synthesizes therapeutic strategies for regulating microglia‐mediated neuroinflammation via FPR modulation, thereby charting a novel course for the treatment of neuroinflammatory diseases. Strategies for targeting FPRs to regulate neuroinflammatory response mediated by microglia. The neuroinflammatory response mediated by microglia can be effectively modulated through the administration of T‐0080 (A), cFLFLF (B), HCH6‐1 (C), and Resveratrol (D) to regulate FPR1 expression. Alternatively, FPR2 agonists such as MR‐39 (E), RvD1 (F), ANXA1 and AC2‐26 (G), LXA4 (H), TGF‐β1 (I), and Boc2 (J) have demonstrated efficacy in this context.