随着癌症患者生存时间的延长，癌症治疗引起的心血管疾病（CVD）的出现已成为人们关注的焦点，成为癌症幸存者的第二大死因。本综述探讨了三种不同类型的程序性细胞死亡（PCD）：铁死亡、铜死亡和全凋亡，重点关注它们在化疗引起的心脏毒性中的作用。铁死亡和铜死亡是由过量的铁和铜 (Cu) 引发的，而 PANoptosis 是一种炎症性 PCD，具有焦亡、细胞凋亡和坏死性凋亡的特征。最近的研究揭示了这些 PCD 类型之间错综复杂的联系，强调了铜死亡和铁死亡之间的相互作用。值得注意的是，细胞内 Cu 通过 GPX4 促进铁死亡的作用得到了强调。此外，ROS 诱导的 PANoptosis 受到铁死亡和铜死亡的影响，表明存在复杂的相互关系。这篇综述提供了对这些 PCD 模式的分子机制及其对化疗引起的心脏毒性的独特贡献的见解。此外，我们还讨论了心脏保护药物在治疗这些 PCD 类型中的潜在应用。这项综合分析旨在促进对与癌症治疗相关的心脏毒性的理解、诊断和治疗策略。版权所有 © 2024。由 Elsevier Ltd 出版。

With the prolonged survival of individuals with cancer, the emergence of cardiovascular diseases (CVD) induced by cancer treatment has become a significant concern, ranking as the second leading cause of death among cancer survivors. This review explores three distinct types of programmed cell death (PCD): ferroptosis, cuproptosis, and PANoptosis, focusing on their roles in chemotherapy-induced cardiotoxicity. While ferroptosis and cuproptosis are triggered by excess iron and copper (Cu), PANoptosis is an inflammatory PCD with features of pyroptosis, apoptosis, and necroptosis. Recent studies reveal intricate connections among these PCD types, emphasizing the interplay between cuproptosis and ferroptosis. Notably, the role of intracellular Cu in promoting ferroptosis through GPX4 is highlighted. Additionally, ROS-induced PANoptosis is influenced by ferroptosis and cuproptosis, suggesting a complex interrelationship. This review provides insights into the molecular mechanisms of these PCD modalities and their distinct contributions to chemotherapy-induced cardiotoxicity. Furthermore, we discuss the potential application of cardioprotective drugs in managing these PCD types. This comprehensive analysis aims to advance the understanding, diagnosis, and therapeutic strategies for cardiotoxicity associated with cancer treatment.Copyright © 2024. Published by Elsevier Ltd.