This review examines the pathophysiological mechanisms of doxorubicin-induced cardiotoxicity and its association with accelerated aging in the heart. Doxorubicin, a widely used chemotherapeutic drug, has been linked to cancer-related cardiac dysfunction (CTRCD), with up to 9% of cancer patients developing heart failure. The review highlights the similarities between the effects of doxorubicin and aging on the heart, including hypertrophy, fibrosis, and increased incidence of atrial fibrillation. It discusses the molecular and biological characteristics of doxorubicin, such as its inhibition of Topoisomerase IIβ and increased reactive oxygen species (ROS) production. The review also explores the accelerated aging phenotype in doxorubicin-treated hearts, including DNA damage, telomere shortening, and cellular senescence. Additionally, it covers the role of mitochondrial dysfunction, calcium flux, and the immune system in the pathogenesis of doxorubicin-induced cardiotoxicity. Finally, the review discusses potential therapeutic strategies, including senolytics and senomorphics, and the importance of biomarkers in predicting outcomes.This review examines the pathophysiological mechanisms of doxorubicin-induced cardiotoxicity and its association with accelerated aging in the heart. Doxorubicin, a widely used chemotherapeutic drug, has been linked to cancer-related cardiac dysfunction (CTRCD), with up to 9% of cancer patients developing heart failure. The review highlights the similarities between the effects of doxorubicin and aging on the heart, including hypertrophy, fibrosis, and increased incidence of atrial fibrillation. It discusses the molecular and biological characteristics of doxorubicin, such as its inhibition of Topoisomerase IIβ and increased reactive oxygen species (ROS) production. The review also explores the accelerated aging phenotype in doxorubicin-treated hearts, including DNA damage, telomere shortening, and cellular senescence. Additionally, it covers the role of mitochondrial dysfunction, calcium flux, and the immune system in the pathogenesis of doxorubicin-induced cardiotoxicity. Finally, the review discusses potential therapeutic strategies, including senolytics and senomorphics, and the importance of biomarkers in predicting outcomes.