Cardiotoxicity induced by traditional chemotherapy: mechanisms and mitigation strategies

Traditional chemotherapeutic agents are indispensable in cancer treatment. However, their therapeutic efficacy is frequently constrained by associated toxicities and adverse effects. Among these adverse effects, cardiotoxicity has emerged as a major clinical concern due to the increasing incidence. Emerging evidence suggests that oxidative stress, programmed cell death pathways, oxidative stress, and inflammatory cascades predominantly mediate the pathogenesis of cardiotoxicity induced by chemotherapeutic agents. Current strategies for monitoring and prevention rely on potential biomarkers, including markers of myocardial injury (e.g., troponins and natriuretic peptides), inflammatory mediators (e.g., myeloperoxidase, interleukin-6, C-reactive protein, and tumor necrosis factor-alpha), and exosomal contents (e.g., microRNAs, proteins, and metabolites). Clinical trials and case reports have demonstrated that patients with chemotherapy-induced cardiotoxicity may benefit from therapeutic interventions such as angiotensin-converting enzyme inhibitors, dexrazoxane, and β-blockers. However, limitations associated with these potential biomarkers and therapeutic agents warrant further discussion because of the lack of solid evidence from large-scale, prospective clinical studies. In summary, further research is imperative to enhance the understanding, monitoring, and therapeutic management of cardiotoxicity associated with traditional chemotherapeutic agents.