Not only does cancer pose a serious threat to longevity, quality of life, and negatively impact social health of individuals worldwide, but various cancer treatments exacerbate this burden through the progression of cardiovascular toxicity. In 2017, startling statistics estimated about 17.8 million deaths worldwide associated with cardiovascular diseases (CVDs) and continues to have an upward trend, suggesting the importance of understanding CVDs and their progression. In this comprehensive review, the prevalence of cardiovascular toxicity will be investigated, and its causes, specifically from cancer treatments. This is particularly important due to numerous cancer treatments like Doxorubicin (DOX) inducing oxidative damage in a non-specific manner targeting healthy cells like cardiomyocytes, leading to atherosclerosis, heart failure, hypertension, arrhythmias, and more debilitating diseases. This review aims to evaluate mechanisms that drive the development of CVDs through cellular death pathways. It also highlights the relevance of potential therapeutic interventions by targeting signals and modulators that contribute to oxidative stress without compromising anti-cancer drug efficacy. Researchers provide remarkable evidence through H9C2 cell samples and animal studies guiding future advancements in clinical pharmacology. For instance, interest has grown in the antioxidant mimetic effects and reduction of lipid peroxidation observed with WGX50 and GC4419.