<p>Cardiotoxicity is the most common side effect of various chemotherapy medications. Doxorubicin (DOX), which belongs to the anthracycline group, belonging to subordinate product produced by the <i>Streptomyces peucetius</i> var. caesius mutant variant. The main mechanisms via which DOX demonstrates its cancer-preventing actions in quickly developing tumours are DNA intercalation along with topoisomerase II enzyme inhibition. However, DOX’s starting point is progressive and dose-specific cardiac toxicity, increasing the possibility of adverse outcomes for cancer individuals as well as limiting its widespread clinical use. Numerous mechanisms have been postulated to explain the cardiotoxicity caused by doxorubicin, but the most often reported ones include oxidative stress, free radical production, mitochondrial malfunction, autophagy, and apoptosis. Other processes, including those involving endothelial cells, smooth muscle cells, inflammation of the heart, along heart fibrosis, are also implicated in the direct implications of DOX on the cardiovascular system. Additionally, a number of compounds have demonstrated promise in preclinical research to lessen these difficulties related to cardiac toxicity. To reduce cardiotoxicity, some inhibitors, antioxidants, plant-based products, and cardioprotective medications have been suggested. As a result, we have given a thorough update on our current knowledge of the pathogenic processes underlying the widely recognised DOX-induced cardiotoxicity in this review. Additionally, we have included a few of the most rational pharmacological approaches that have been tried to prevent toxicity of the heart induced by DOX.</p> Graphical Abstract <p></p>