铁死亡是一种由铁依赖性磷脂（PL）过氧化驱动的新型细胞死亡模式，已成为治疗癌症、心血管疾病和缺血再灌注损伤（IRI）的一种有前景的治疗策略。 PL过氧化是铁死亡的关键过程，需要含有多不饱和脂肪酸（PUFA）的PL（PL-PUFA）作为底物，与铁和氧发生链式反应。细胞通过维持底物、过程和 PL 过氧化解毒之间的稳态平衡来预防铁死亡。细胞膜中丰富的甾醇类脂质直接参与 PL 过氧化并影响铁死亡敏感性。甾醇代谢在铁死亡中也起着关键作用，靶向甾醇在治疗多种铁死亡相关疾病方面具有巨大潜力。这篇综述阐明了铁死亡的基本机制，强调了甾醇如何调节这一过程及其治疗潜力。版权所有 © 2024 Elsevier Ltd. 保留所有权利。

Ferroptosis, a novel cell death mode driven by iron-dependent phospholipid (PL) peroxidation, has emerged as a promising therapeutic strategy for the treatments of cancer, cardiovascular diseases, and ischemic-reperfusion injury (IRI). PL peroxidation, the key process of ferroptosis, requires polyunsaturated fatty acid (PUFA)-containing PLs (PL-PUFAs) as substrates, undergoing a chain reaction with iron and oxygen. Cells prevent ferroptosis by maintaining a homeostatic equilibrium among substrates, processes, and detoxification of PL peroxidation. Sterols, lipids abundant in cell membranes, directly participate in PL peroxidation and influence ferroptosis sensitivity. Sterol metabolism also plays a key role in ferroptosis, and targeting sterols presents significant potential for treating numerous ferroptosis-associated disorders. This review elucidates the fundamental mechanisms of ferroptosis, emphasizing how sterols modulate this process and their therapeutic potential.Copyright © 2024 Elsevier Ltd. All rights reserved.