Key points are not available for this paper at this time.
BACKGROUND: Spinal cord injury (SCI) initiates a cascade of secondary pathological processes significantly impairs functional recovery and leads to complications such as neuropathic pain. Arachidonic acid (AA) and its metabolites play crucial roles through various metabolic pathways. These pathways contribute to neuroinflammation, tissue damage, and functional impairment following SCI. AIM: We aim to provide a comprehensive outline on AA metabolic pathways, enzymes and signaling cascades in spinal cord injury pathophysiology, in order to develop new perspectives in treatment and diagnosis. KEY SCIENTIFIC CONCEPTS: We present a comprehensive review on AA metabolism and pathways in the different pathology process of SCI, such as neuronal loss, demyelination, neuropathic pain and neuroinflammation with different cell types involved. We also discussed the complex interactions of AA metabolites pose challenges for the development of effective therapies. Finally, we outlooked future research directions aimed at optimizing AA-targeted treatments and expanding their clinical applicability to enhance recovery in patients with SCI.
Yao et al. (Sat,) studied this question.