Production and Role of Free Radicals and Reactive Oxygen Species After Facial Nerve Injury

Facial nerve injury (FNI) induces complex molecular and cellular responses, with reactive oxygen species (ROS) and free radicals (FRs) playing pivotal roles in nerve degeneration and regeneration. However, to date, no systematic review has specifically investigated the involvement of ROS and FRs in FNI. To address this unmet need, we reviewed the literature on the subject, comprehensively searching SCOPUS, PubMed, Cochrane Library, EMBASE, and Google Scholar to identify studies that assessed the roles of FRs and ROS in FNI and summarize their findings. A total of 15 studies that satisfied search criteria were identified. Key findings showed that excessive ROS and FR lead to mitochondrial dysfunction, lipid peroxidation, and ferroptosis, exacerbating nerve degeneration after facial nerve injury. These effects are modulated by antioxidants, including alpha-lipoic acid, edaravone, N(ω)-nitro-L-arginine methyl ester (L-NAME), glutathione peroxidase 4, glutathione, methylprednisolone sodium succinate, Si-based agents, superoxide dismutase, and tirilazad mesylate. The insights gained from this review suggest that levels of FRs and ROS are strongly associated with the pathophysiology of facial nerve injury and underscore the therapeutic potential of targeting ROS and FR pathways in facial nerve injuries.