Ferroptosis, a recently identified and iron-dependent cell death, differs from other cell death such as apoptosis, necroptosis, pyroptosis, and autophagy-dependent cell death. This form of cell death does not exhibit typical morphological and biochemical characteristics, including cell shrinkage, mitochondrial fragmentation, nuclear condensation. The dysfunction of lipid peroxide clearance, the presence of redox-active iron as well as oxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids are three essential features of ferroptosis. Iron metabolism and lipid peroxidation signaling are increasingly recognized as central mediators of ferroptosis. Ferroptosis plays an important role in the regulation of oxidative stress and inflammatory responses. Accumulating evidence suggests that ferroptosis is implicated in a variety of cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure, indicating that targeting ferroptosis will present a novel therapeutic approach against cardiovascular diseases. Here, we provide an overview of the features, process, function, and mechanisms of ferroptosis, and its increasingly connected relevance to oxidative stress, inflammation, and cardiovascular diseases.

铁死亡是一种最近发现的铁依赖性细胞死亡，不同于其他细胞死亡，如细胞凋亡、坏死性凋亡、细胞焦亡和自噬依赖性细胞死亡。这种细胞死亡形式不表现出典型的形态和生化特征，包括细胞收缩、线粒体断裂、核浓缩。脂质过氧化物清除功能障碍、氧化还原活性铁的存在以及含多不饱和脂肪酸 (PUFA) 的磷脂氧化是铁死亡的三个基本特征。铁代谢和脂质过氧化信号越来越被认为是铁死亡的中心介质。铁死亡在氧化应激和炎症反应的调节中起重要作用。越来越多的证据表明，铁死亡与动脉粥样硬化、中风、缺血再灌注损伤和心力衰竭等多种心血管疾病有关，表明以铁死亡为靶点将提供一种新的心血管疾病治疗方法。在这里，我们概述了铁死亡的特征、过程、功能和机制，以及它与氧化应激、炎症和心血管疾病日益密切的相关性。