Abstract：
Doxorubicin (DOX) is an anti-tumor agent for chemotherapy, but its use is often hindered by the severe and life-threatening side effect of cardiovascular toxicity. In recent years, studies have focused on dysregulated iron metabolism and ferroptosis, a unique type of cell death induced by iron overload, as key players driving the development of DOX-induced cardiotoxicity (DIC). Recent advances have demonstrated that DOX disturbs normal cellular iron metabolism, resulting in excessive iron accumulation and ferroptosis in cardiomyocytes. This review will explore how dysregulated iron homeostasis and ferroptosis drive the progression of DIC. We will also discuss the current approaches to target iron metabolism and ferroptosis to mitigate DIC. Besides, we will discuss the limitations and challenges for clinical translation for these therapeutic regimens.
摘要：
多柔比星（DOX）是一种用于化疗的抗肿瘤药物，但它的使用往往受到严重和危及生命的心血管毒性副作用的阻碍。近年来,研究集中在铁代谢失调和铁凋亡，铁过载诱导的一种独特类型的细胞死亡，作为推动DOX诱导的心脏毒性（DIC）发展的关键参与者。最近的进展表明，DOX扰乱正常的细胞铁代谢，导致心肌细胞中铁的过度积累和铁凋亡。这篇综述将探讨铁稳态失调和铁凋亡如何驱动DIC的进展。我们还将讨论目前靶向铁代谢和铁凋亡以减轻DIC的方法。此外,我们将讨论这些治疗方案在临床转化方面的局限性和挑战.
