作为化疗药物，阿霉素用于对抗癌症。然而，心脏毒性限制了其使用。现有策略无法消除阿霉素引起的心脏毒性，迫切需要深入探讨其发病机制来解决这一问题。当内质网 (ER) 功能障碍导致未折叠或错误折叠蛋白质的积累时，就会发生内质网应激 (ERS)。适应性ERS有助于调节蛋白质合成以维持细胞稳态，而长时间的ERS刺激可能诱导细胞凋亡，导致组织和器官功能障碍和损伤。关于阿霉素诱导的心脏毒性的大量研究表明，ERS 的过度激活与氧化应激、钙失衡、自噬、泛素化和细胞凋亡等机制密切相关。研究人员还发现几种临床药物、化合物、植物化学物质和 miRNA 通过靶向 ERS ​​抑制阿霉素诱导的心脏毒性。本综述旨在概述 ERS ​​与阿霉素诱导的心脏毒性中其他机制之间的相互作用，并总结 ERS ​​在此类心脏毒性中的作用。此外，该综述列举了几种针对 ERS ​​的临床药物、植物化学物质、化合物和 miRNA，以考虑解决阿霉素引起的心脏毒性的治疗方案。版权所有 © 2024 Sun、Zhang、Tan、Zhang、Zhao 和 Dong。

As a chemotherapy agent, doxorubicin is used to combat cancer. However, cardiotoxicity has limited its use. The existing strategies fail to eliminate doxorubicin-induced cardiotoxicity, and an in-depth exploration of its pathogenesis is in urgent need to address the issue. Endoplasmic reticulum stress (ERS) occurs when Endoplasmic Reticulum (ER) dysfunction results in the accumulation of unfolded or misfolded proteins. Adaptive ERS helps regulate protein synthesis to maintain cellular homeostasis, while prolonged ERS stimulation may induce cell apoptosis, leading to dysfunction and damage to tissue and organs. Numerous studies on doxorubicin-induced cardiotoxicity strongly link excessive activation of the ERS to mechanisms including oxidative stress, calcium imbalance, autophagy, ubiquitination, and apoptosis. The researchers also found several clinical drugs, chemical compounds, phytochemicals, and miRNAs inhibited doxorubicin-induced cardiotoxicity by targeting ERS. The present review aims to outline the interactions between ERS and other mechanisms in doxorubicin-induced cardiotoxicity and summarize ERS's role in this type of cardiotoxicity. Additionally, the review enumerates several clinical drugs, phytochemicals, chemical compounds, and miRNAs targeting ERS for considering therapeutic regimens that address doxorubicin-induced cardiotoxicity.Copyright © 2024 Sun, Zhang, Tan, Zhang, Zhao and Dong.