Many new types of regulated cell death have been recently implicated in human health and disease. These regulated cell deaths have different morphological, genetic, biochemical, and functional hallmarks. Ferroptosis was originally described as a carcinogenic RAS-dependent non-apoptotic cell death, and is now defined as a type of regulated necrosis characterized by iron accumulation, lipid peroxidation, and the release of damage-associated molecular patterns (DAMPs). Multiple oxidative and antioxidant systems, acting together autophagy machinery, shape the process of lipid peroxidation during ferroptosis. In particular, the production of reactive oxygen species (ROS) that depends on the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and the mitochondrial respiratory chain promotes lipid peroxidation by lipoxygenase (ALOX) or cytochrome P450 reductase (POR). In contrast, the glutathione (GSH), coenzyme Q10 (CoQ10), and tetrahydrobiopterin (BH₄) system limits oxidative damage during ferroptosis. These antioxidant processes are further transcriptionally regulated by nuclear factor, erythroid 2-like 2 (NFE2L2/NRF2), whereas membrane repair during ferroptotic damage requires the activation of endosomal sorting complexes required for transport (ESCRT)-III. A further understanding of the process and function of ferroptosis may provide precise treatment strategies for disease.

最近，许多新型的受调节细胞死亡与人类健康和疾病有关。这些受调节的细胞死亡具有不同的形态、遗传、生化和功能特征。铁死亡最初被描述为一种致癌的 RAS 依赖性非凋亡细胞死亡，现在被定义为一种以铁积累、脂质过氧化和损伤相关分子模式 (DAMP) 释放为特征的调节性坏死。多种氧化和抗氧化系统与自噬机制共同作用，塑造了铁死亡过程中的脂质过氧化过程。特别是，活性氧 (ROS) 的产生取决于烟酰胺腺嘌呤二核苷酸磷酸 (NADPH) 氧化酶 (NOX) 和线粒体呼吸链的活性，通过脂氧合酶 (ALOX) 或细胞色素 P450 还原酶 (POR) 促进脂质过氧化。相比之下，谷胱甘肽 (GSH)、辅酶 Q10 (CoQ10) 和四氢生物蝶呤 (BH ₄ ) 系统可限制铁死亡过程中的氧化损伤。这些抗氧化过程进一步受到核因子红细胞 2 样 2 (NFE2L2/NRF2) 的转录调节，而铁死亡损伤期间的膜修复需要激活转运所需的内体分选复合物 (ESCRT)-III。对铁死亡过程和功能的进一步了解可能为疾病提供精准的治疗策略。