铁死是一种由铁依赖型脂质过氧化引起的调节性细胞死亡形式。该过程在各种人类疾病中导致细胞和组织损伤，如心血管疾病、神经变性、肝病和癌症。尽管磷脂膜中的多不饱和脂肪酸（PUFAs）优先被氧化，但饱和/单不饱和脂肪酸（SFAs / MUFAs）也影响脂质过氧化和铁死。在本综述中，我们首先解释了细胞如何差异化合成SFA / MUFAs和PUFAs以及它们如何通过脂肪酸摄取和β-氧化控制脂肪酸池，从而影响铁死。此外，我们还讨论了脂肪酸如何存储在不同的脂质中，如具有不同头基的二酰基或醚磷脂，三酸甘油脂和胆固醇。此外，我们解释了这些脂肪酸如何从这些分子中释放出来。总之，我们通过重新审视脂质组学研究，提供了与铁死相关的多样化和动态代谢过程的整体视角。因此，本综述为铁死相关疾病的治疗策略的开发做出了贡献。© 2023. 作者。

Ferroptosis is a form of regulated cell death characterized by iron-dependent lipid peroxidation. This process contributes to cellular and tissue damage in various human diseases, such as cardiovascular diseases, neurodegeneration, liver disease, and cancer. Although polyunsaturated fatty acids (PUFAs) in membrane phospholipids are preferentially oxidized, saturated/monounsaturated fatty acids (SFAs/MUFAs) also influence lipid peroxidation and ferroptosis. In this review, we first explain how cells differentially synthesize SFA/MUFAs and PUFAs and how they control fatty acid pools via fatty acid uptake and β-oxidation, impacting ferroptosis. Furthermore, we discuss how fatty acids are stored in different lipids, such as diacyl or ether phospholipids with different head groups; triglycerides; and cholesterols. Moreover, we explain how these fatty acids are released from these molecules. In summary, we provide an integrated view of the diverse and dynamic metabolic processes in the context of ferroptosis by revisiting lipidomic studies. Thus, this review contributes to the development of therapeutic strategies for ferroptosis-related diseases.© 2023. The Author(s).