FGF21 prevents neuronal cell ferroptosis after spinal cord injury by activating the FGFR1/β-Klotho pathway

脊髓损伤 医学 脊髓 纺神星 程序性细胞死亡 细胞凋亡 神经科学 内分泌学 生物 生物化学
作者
Tianli Xu,Qiancheng Zhu,Qun Huang,Qi Gu,Zhu Yi,Mengjie Tang,Shoujin Tian,Liming Wang,Fei Yan,Jianfei Ge,Xiaolong Lin,Xiaolong Lin
出处
期刊:Brain Research Bulletin [Elsevier]
卷期号:202: 110753-110753 被引量:5
标识
DOI:10.1016/j.brainresbull.2023.110753
摘要

Spinal cord injury (SCI) is a kind of traumatic nervous system disease caused by neuronal death, causing symptoms like sensory, motor, and autonomic nerve dysfunction. The recovery of neurological function has always been a intractable problem that has greatly distressed individuals and society. Although the involvement of iron-dependent lipid peroxidation leading to nerve cell ferroptosis in SCI progression has been reported, the underlying mechanisms remain unaddressed. Thus, this study aimed to investigate the potential of recombinant human FGF21 (rhFGF21) in inhibiting ferroptosis of nerve cells and improving limb function after SCI, along with its underlying mechanisms. In vivo animal model showed that FGFR1, p-FGFR1, and β-Klotho protein gradually increased over time after injury, reaching a peak on the third day. Moreover, rhFGF21 treatment significantly reduced ACSL4, increased GPX4 expression, reduced iron deposition, and inhibited ferroptosis. Meanwhile, rhFGF21 decreased cell apoptosis following acute spinal cord damage. In contrast, FGFR1 inhibitor PD173074 partially reversed the rhFGF21-induced therapeutic effects. Overall, this work revealed that rhFGF21 activates the FGFR1/β-Klotho pathway to decrease ferroptosis of nerve cells, suggesting that FGF21 could be a new therapeutic target for SCI neurological rehabilitation.
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