Fibroblast growth factor 17 modulates neuroinflammation and promotes recovery after traumatic spinal cord injury

Cervical spinal cord injuries result in impairments to both the cardiovascular and respiratory systems. Following the initial traumatic injury, secondary processes trigger neuroinflammation and demyelination, which exacerbate lesion expansion impairing functional recovery. Alteration in astrocyte and oligodendrocyte signaling contribute to this pathology, with astrocytes driving scar formation and impairments in oligodendrocytes resulting in loss of myelin integrity. Fibroblast growth factor 17 (FGF17), a naturally occurring ligand with high affinity for FGF receptors 3 and 4, shows promise for modulating these processes. Notably, overexpression of FGFR4 in astrocytes has been linked to improved locomotor function after thoracic injury, while activation of FGFR3 by FGF17 has been shown to promote oligodendrogenesis and enhance working memory. Here we investigate how FGF17 administration during the acute phase following spinal cord injury could act to restore function. FGF17 treatment within the first week following injury mitigated transient hypertension induced by colorectal distension, a hallmark of autonomic dysreflexia. Additionally, FGF17 improved ventilation by attenuating tidal volume reductions after cervical SCI. These functional improvements correlated with increased tissue sparing at the injury site. Ongoing studies aim to elucidate the cellular and molecular mechanisms underlying these protective effects. These findings highlight the potential of FGF17 to mitigate secondary injury cascades and promote functional recovery, particularly in addressing cardiorespiratory dysfunction following SCI. Craig H. Neilsen Foundation SCIRTS Post-Doctoral Fellowship (MDS), Kentucky Spinal Cord and Head Injury Research Trust (WJA) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.