Ferroptosis plays a pivotal role in regulating various physiological processes and quality of post-mortem muscle. However, the molecular mechanisms underlying ferroptosis remain unclear. The study investigated how ferroptosis was induced in beef during cold storage. Results showed that the expression of autophagy-related genes, LC3, ATG5, ATG7, and NCOA4 in beef during cold storage promoted the degradation of ferritin heavy chains. Ferritin evoked ferroptosis by releasing free iron, inducing reactive oxygen species (ROS) accumulation and inhibiting the glutathione (GSH)-glutathione peroxidase 4 (GPX4) pathway. Furthermore, treatment of myoblasts with GSK 2656157 (autophagy inhibitor) showed that ferritin degradation was lower in the GSK 2656157-treated myoblasts than in the control, while GSH content and GPX4 activity were higher than the control (P < 0.05), and the contents of free iron, ROS and malondialdehyde, and apoptosis were lower than the control (P < 0.05). These results suggest that ferroptosis is induced by degradation of ferritin via the autophagic pathway.

铁死亡在调节各种生理过程和死后肌肉质量方面起着举足轻重的作用。然而，铁死亡的分子机制仍不清楚。该研究调查了牛肉在冷藏过程中如何诱发铁死亡。结果表明，牛肉冷藏过程中自噬相关基因LC3、ATG5、ATG7和NCOA4的表达促进了铁蛋白重链的降解。铁蛋白通过释放游离铁、诱导活性氧 (ROS) 积累和抑制谷胱甘肽 (GSH)-谷胱甘肽过氧化物酶 4 (GPX4) 通路来诱发铁死亡。此外，用 GSK 2656157（自噬抑制剂）处理成肌细胞表明，GSK 2656157 处理的成肌细胞中铁蛋白降解低于对照组，而 GSH 含量和 GPX4 活性高于对照组（P  < 0.05），游离铁、ROS 和丙二醛含量、细胞凋亡均低于对照（P  < 0.05）。这些结果表明铁死亡是由铁蛋白通过自噬途径降解引起的。