Activation of PAR1 contributes to ferroptosis of Schwann cells and inhibits regeneration of myelin sheath after sciatic nerve crush injury in rats via Hippo-YAP/ACSL4 pathway

Peripheral nerve injury (PNI) is characterized by high incidence and sequela rate. Recently, there was increasing evidence that has shown ferroptosis may impede functional recovery. Our objective is to explore the novel mechanism that regulates ferroptosis after PNI. LC-MS/MS proteomics was used to...

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Veröffentlicht in:	Experimental neurology 2025-02, Vol.384, p.115053, Article 115053
Hauptverfasser:	Wu, Zhimin, Sun, Jun, Liao, Zhi, Sun, Tao, Huang, Lixin, Qiao, Jia, Ling, Cong, Chen, Chuan, Zhang, Baoyu, Wang, Hui
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Crush Injuries Ferroptosis Ferroptosis - drug effects Ferroptosis - physiology Hippo-YAP pathway Male Myelin Sheath - metabolism Myelin Sheath - pathology Nerve Crush Nerve Regeneration - drug effects Nerve Regeneration - physiology Peripheral Nerve Injuries - metabolism Peripheral nerve injury (PNI) Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Rats Rats, Sprague-Dawley Receptor, PAR-1 - genetics Receptor, PAR-1 - metabolism Regeneration of myelin sheath Schwann cell (SC) Schwann Cells - metabolism Sciatic Nerve - injuries Signal Transduction - drug effects Signal Transduction - physiology YAP-Signaling Proteins
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