Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis

The intricate pathophysiological cascades following spinal cord injury (SCI), encompassing cellular demise, axonal degeneration, and the formation of glial scars, pose formidable barriers to neural regeneration and restoration. Notably, neuroinflammation and glial scars emerge as pivotal barrier to post-SCI repair. Formyl peptide receptors (FPRs) emerge as critical regulators of immune responses, exerting significant influence over inflammatory modulation and nerve regeneration subsequent to SCI. Beyond their classical expression in myeloid cells, FPRs demonstrate a pronounced presence within the central nervous system (CNS) with roles in the progression of neurodegenerative disorders and neurological malignancies. Post-SCI, the equilibrium of the inflammatory microenvironment is recalibrated through the strategic modulation of FPRs, including facilitating a balance in microglial polarization, stimulating neural stem cells (NSCs) migration, and promoting neural axon elongation. These observations enlighten the potential of FPRs as innovative targets for neuronal regenerations bolstering SCI repair. This review endeavors to delineate the distribution and function of FPRs in the aftermath of SCI, with a special attention to their roles in inflammatory regulation, NSCs mobilization, and synaptic growth. By elucidating these mechanisms, we aspire to contribute novel insights and strategies for SCI therapy.