铁死亡(ferroptosis)是一种与铁代谢异常和脂质过氧化物过量累积有关的调节性细胞死亡方式,具有独特的生物学过程和病理生理特征。脂质过氧化是铁死亡发生的最主要机制之一。越来越多的证据表明,铁死亡在肿瘤的发生发展与治疗过程中发挥重要的调节作用。诱导肿瘤细胞铁死亡可有效抑制肿瘤的生长和转移,提高抗肿瘤药物的治疗敏感性。本文通过综述磷脂的合成和重塑、磷脂的储存和释放、脂肪酸的摄取和氧化等脂质代谢方式调控铁死亡的机制,总结脂质代谢相关的信号通路对铁死亡的影响及针对相关靶点的治疗策略,为铁死亡相关基础研究与肿瘤临床治疗提供新的思路。

Ferroptosis is a form of programmed cell death associated with abnormal iron metabolism and excessive accumulation of lipid peroxides, characterized by unique biological processes and pathophysiological features. Lipid peroxidation represents the most fundamental mechanism underlying ferroptosis. Increasing evidence indicates that ferroptosis plays significant regulatory roles in the onset, development, and treatment of tumors.Induction of ferroptosis in tumor cells can effectively inhibit tumor growth and metastasis, and improve the therapeutic sensitivity of anti-tumor drugs. This article reviews the mechanisms by which lipid metabolic processes, such as the synthesis and remodeling of phospholipids,the storage and release of phospholipids,as well as the uptake and oxidation of fatty acids,regulate ferroptosis.It summarizes the effects of lipid metabolism-associated signaling pathways on ferroptosis and targeted therapeutic strategies, aiming to provide new insights for ferroptosis-associated basic research and clinical tumor therapy.