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Fibroblast growth factor 21 (\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21) is a metabolic factor that regulates blood glucose and lipid homeostasis. However, there is little concern for the potential protective effect of\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21 on nerve regeneration after\n                    <jats:styled-content style=\"fixed-case\">PNI<\/jats:styled-content>\n                    and revealing related molecular mechanisms. Here, we firstly found that exogenous\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21 administration remarkably promoted functional and morphologic recovery in a rat model of sciatic crush injury, manifesting as persistently improved motor and sensory function, enhanced axonal remyelination and regrowth and accelerated Schwann cells (\n                    <jats:styled-content style=\"fixed-case\">SC<\/jats:styled-content>\n                    s) proliferation. Furthermore, local\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21 application attenuated the excessive activation of oxidative stress, which was accompanied with the activation of nuclear factor erythroid\u20102\u2010related factor 2 (Nrf\u20102) transcription and extracellular regulated protein kinases (\n                    <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>\n                    ) phosphorylation. We detected\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21 also suppressed autophagic cell death in\n                    <jats:styled-content style=\"fixed-case\">SC<\/jats:styled-content>\n                    s. Additionally, treatment with the\n                    <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>\n                    inhibitor U0126 or autophagy inhibitor 3\u2010\n                    <jats:styled-content style=\"fixed-case\">MA<\/jats:styled-content>\n                    partially abolishes anti\u2010oxidant effect and reduces\n                    <jats:styled-content style=\"fixed-case\">SC<\/jats:styled-content>\n                    s death. Taken together, these results indicated that the role of\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21 in remyelination and nerve regeneration after\n                    <jats:styled-content style=\"fixed-case\">PNI<\/jats:styled-content>\n                    was probably related to inhibit the excessive activation of\n                    <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>\n                    \/Nrf\u20102 signalling\u2010regulated oxidative stress and autophagy\u2010induced cell death. Overall, our work suggests that\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    21 administration may provide a new therapy for\n                    <jats:styled-content style=\"fixed-case\">PNI<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/jcmm.13952","type":"journal-article","created":{"date-parts":[[2018,11,19]],"date-time":"2018-11-19T01:44:19Z","timestamp":1542591859000},"page":"497-511","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":73,"title":["Fibroblast growth factor 21 facilitates peripheral nerve regeneration through suppressing oxidative damage and autophagic cell death"],"prefix":"10.1111","volume":"23","author":[{"given":"Yingfeng","family":"Lu","sequence":"first","affiliation":[{"name":"Department of Hand Surgery and Peripheral Neurosurgery The First Affiliated Hospital of Wenzhou Medical University 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