Neurofascin stabilization by contactin-associated protein-like 2 and CTCF alleviates mitochondrial dysfunction in Schwann cells during facial nerve injury.

ABSTRACT: During the growth or treatment of oral and maxillofacial tumors, the facial nerve is susceptible to injury, resulting facial dysfunction. Iodine-125 (I-125) seed brachytherapy is widely used in the treatment of various tumors due to its precise and sustained radiation characteristics, yet it may also cause nerve damage. However, the underlying mechanism of I-125 seed implantation-induced facial nerve injury (FNI) remains unclear. Here, a rabbit FNI model was established, and the neural injury mechanism was further investigated through I-125 seed implantation combined with transcriptome sequencing. Results found that neurofascin (NFASC) expression was reduced in injured rabbit facial nerves, and the implantation of I-125 particles further decreased NFASC expression. Overexpression of NFASC

SUBMITTER: Zhu J 

PROVIDER: S-EPMC12818255 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature