Anthracyclines (ANTs) are a class of anticancer drugs widely used in oncology. However, the clinical application of ANTs is limited by their cardiotoxicity. The mechanisms underlying ANTs-induced cardiotoxicity (AIC) are complicated and involve oxidative stress, inflammation, topoisomerase 2β inhibition, pyroptosis, immunometabolism, autophagy, apoptosis, ferroptosis, etc. Ferroptosis is a new form of regulated cell death (RCD) proposed in 2012, characterized by iron-dependent accumulation of reactive oxygen species (ROS) and lipid peroxidation. An increasing number of studies have found that ferroptosis plays a vital role in the development of AIC. Therefore, we aimed to elaborate on ferroptosis in AIC, especially by doxorubicin (DOX). We first summarize the mechanisms of ferroptosis in terms of oxidation and anti-oxidation systems. Then, we discuss the mechanisms related to ferroptosis caused by DOX, particularly from the perspective of iron metabolism of cardiomyocytes. We also present our research on the prevention and treatment of AIC based on ferroptosis. Finally, we enumerate our views on the development of drugs targeting ferroptosis in this emerging field.

As a result of ongoing breakthroughs in cancer therapy, cancer patients' survival rates have grown considerably. However, cardiotoxicity has emerged as the most dangerous toxic side effect of cancer treatment, negatively impacting cancer patients' prognosis. In recent years, the link between non-coding RNAs (ncRNAs) and cancer therapy-induced cardiotoxicity has received much attention and investigation. NcRNAs are non-protein-coding RNAs that impact gene expression post-transcriptionally. They include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). In several cancer treatments, such as chemotherapy, radiotherapy, and targeted therapy-induced cardiotoxicity, ncRNAs play a significant role in the onset and progression of cardiotoxicity. This review focuses on the mechanisms of ncRNAs in cancer therapy-induced cardiotoxicity, including apoptosis, mitochondrial damage, oxidative stress, DNA damage, inflammation, autophagy, aging, calcium homeostasis, vascular homeostasis, and fibrosis. In addition, this review explores potential ncRNAs-based biomarkers and therapeutic strategies, which may help to convert ncRNAs research into clinical practice in the future for early detection and improvement of cancer therapy-induced cardiotoxicity.