Advances in anticancer therapies have substantially improved cancer survival but have also highlighted the growing challenge of cancer therapy-related cardiac dysfunction. Ferroptosis, an iron-dependent form of regulated cell death characterized by iron dysregulation, lipid peroxidation, and impaired antioxidant defense, has emerged as a promising strategy for eliminating therapy-resistant tumors. However, the lack of tissue specificity in ferroptosis regulation raises concerns regarding its potential contribution to cardiovascular injury during anticancer treatment. This review summarizes the dual roles of ferroptosis in cancer biology and cardio-oncology. We first discuss the molecular mechanisms governing ferroptosis, including iron metabolism, lipid peroxidation, and antioxidant defense systems. We then highlight the context-dependent roles of ferroptosis in tumor progression, immune regulation, and metabolic adaptation. Furthermore, we systematically review how chemotherapy, targeted therapy, immunotherapy, and radiotherapy contribute to ferroptosis-associated cardiovascular toxicity. Finally, we discuss emerging approaches to minimize cardiac injury, including tissue-specific ferroptosis-targeting and cardioprotective strategies. Understanding tissue-specific ferroptosis regulation may facilitate the development of safer and more precise therapeutic approaches in cardio-oncology.