The maintenance of iron homeostasis is essential for proper cardiac function. A growing body of evidence suggests that iron imbalance is the common denominator in many subtypes of cardiovascular disease. In the past 10 years, ferroptosis, an iron-dependent form of regulated cell death, has become increasingly recognized as an important process that mediates the pathogenesis and progression of numerous cardiovascular diseases, including atherosclerosis, drug-induced heart failure, myocardial ischaemia–reperfusion injury, sepsis-induced cardiomyopathy, arrhythmia and diabetic cardiomyopathy. Therefore, a thorough understanding of the mechanisms involved in the regulation of iron metabolism and ferroptosis in cardiomyocytes might lead to improvements in disease management. In this Review, we summarize the relationship between the metabolic and molecular pathways of iron signalling and ferroptosis in the context of cardiovascular disease. We also discuss the potential targets of ferroptosis in the treatment of cardiovascular disease and describe the current limitations and future directions of these novel treatment targets.

维持铁稳态对于正常的心脏功能至关重要。越来越多的证据表明，铁失衡是许多心血管疾病亚型的共同点。在过去的10年里，铁死亡（一种铁依赖性调节细胞死亡形式）已被越来越多地认为是介导多种心血管疾病发病机制和进展的重要过程，包括动脉粥样硬化、药物引起的心力衰竭、心肌缺血再灌注损伤、脓毒症引起的心肌病、心律失常和糖尿病心肌病。因此，彻底了解心肌细胞铁代谢和铁死亡的调节机制可能会改善疾病管理。在这篇评论中，我们总结了心血管疾病背景下铁信号传导和铁死亡之间的代谢和分子途径之间的关系。我们还讨论了铁死亡在心血管疾病治疗中的潜在靶点，并描述了这些新治疗靶点的当前局限性和未来方向。