Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death caused by lipid peroxidation, which is controlled by integrated oxidation and antioxidant systems. The iron-containing enzyme lipoxygenase is the main promoter of ferroptosis by producing lipid hydroperoxides, and its function relies on the activation of ACSL4-dependent lipid biosynthesis. In contrast, the selenium-containing enzyme GPX4 is currently recognized as a central repressor of ferroptosis, and its activity depends on glutathione produced from the activation of the cystine-glutamate antiporter SLC7A11. Many metabolic (especially involving iron, lipids, and amino acids) and degradation pathways (macroautophagy/autophagy and the ubiquitin-proteasome system) orchestrate the complex ferroptotic response through direct or indirect regulation of iron accumulation or lipid peroxidation. Although the detailed mechanism of membrane injury during ferroptosis remains a mystery, ESCRT III-mediated plasma membrane repair can make cells resistant to ferroptosis. Here, we review the recent rapid progress in understanding the molecular mechanisms of ferroptosis and focus on the epigenetic, transcriptional, and posttranslational regulation of this process.

Ferroptosis是由脂质过氧化引起的铁依赖性非凋亡形式的受调节的细胞死亡，脂质过氧化受整合的氧化和抗氧化剂系统控制。含铁酶脂氧合酶是通过产生脂质氢过氧化物来促进肥大病的主要启动子，其功能依赖于依赖ACSL4的脂质生物合成的激活。相反，目前已将含硒的酶GPX4视为肥大症的中央阻遏物，其活性取决于胱氨酸-谷氨酸逆转运蛋白SLC7A11的活化所产生的谷胱甘肽。许多新陈代谢（尤其是铁，脂质，和氨基酸）和降解途径（自噬/自噬和泛素-蛋白酶体系统）通过直接或间接调节铁蓄积或脂质过氧化作用来协调复杂的促铁反应。尽管在肥大症的过程中膜损伤的详细机制仍然是一个谜，但ESCRT III介导的质膜修复可以使细胞对肥大症产生抗性。在这里，我们回顾了最近的快速进展，以了解受精症的分子机制，并着重于此过程的表观遗传，转录和翻译后调控。