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However, it remains unclear whether c\u2010Jun can be involved in nerve repair by regulating ferroptosis. To explore this, we first set up a facial nerve injury model and detected the changes of ferroptosis\u2010related proteins and c\u2010Jun by immunofluorescence and Western blot. Then, we cultured RSC 96 and pSCs, and studied the potential regulatory relationships by a combination of experimental methods such as CCK\u20108, ELISA, immunofluorescence, qRT\u2010PCR, Western blot and viral transfection. Finally, we corroborated the role of c\u2010Jun through animal experiments. Our experiments revealed that ferroptosis occurs after facial nerve injury. Erastin decreased GPX4, c\u2010Jun proteins and GSH content, while PTGS2, NRF2, HO\u20101 proteins, MDA, Fe<jats:sup>2+<\/jats:sup> and ROS contents increased. This effect was inhibited after c\u2010Jun overexpression but was reversed after the addition of c\u2010Jun siRNA. Besides, we proved in vivo that c\u2010Jun could inhibit ferroptosis and promote the recovery of facial nerve function. In conclusion, our study identified the relationship between c\u2010Jun and ferroptosis during peripheral nerve injury repair, which provides new ideas for studying peripheral nerve injury and repair.<\/jats:p>","DOI":"10.1111\/jcmm.17241","type":"journal-article","created":{"date-parts":[[2022,2,22]],"date-time":"2022-02-22T09:41:27Z","timestamp":1645522887000},"page":"2191-2204","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Overexpression of c\u2010Jun inhibits erastin\u2010induced ferroptosis in Schwann cells and promotes repair of facial nerve function"],"prefix":"10.1111","volume":"26","author":[{"given":"Dekun","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Otorhinolaryngology\u2010Head and Neck Surgery Xinhua Hospital Shanghai Jiaotong University School of Medicine  Shanghai China"},{"name":"Shanghai Jiaotong University School of Medicine Ear Institute  Shanghai 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