Multidimensional perspectives on cancer therapy-induced cardiotoxicity: Characteristics, mechanisms, biomarkers, psychological stress effects, and treatment progress.
This review synthesizes reported cardiotoxic phenotypes, mechanisms, candidate biomarkers, psychological-stress effects, and emerging management strategies across chemotherapy, targeted therapy, immunotherapy, and radiotherapy, while noting the need for tailored approaches in pediatric patients.
Open original publication →What the AI sees
This review synthesizes reported cardiotoxic phenotypes, mechanisms, candidate biomarkers, psychological-stress effects, and emerging management strategies across chemotherapy, targeted therapy, immunotherapy, and radiotherapy, while noting the need for tailored approaches in pediatric patients.
Research significance
The reviewed evidence suggests that integrating cardiac biomarkers with therapy-specific mechanisms and psychological-stress assessment could support earlier detection and personalized mitigation of cancer therapy-induced cardiotoxicity; however, the supplied record does not establish the efficacy, safety, or pediatric benefit of any specific intervention.
Source abstract
Cancer therapy-induced cardiotoxicity (CTIC) is an unavoidable complication in the treatment of cancer patients, an important issue that threatens their quality of life and long-term prognosis. This review comprehensively summarizes the characteristics, mechanisms, biomarkers, psychological stress (PS)-related exacerbation, and therapeutic advances of cancer therapy-induced cardiotoxicity (CTIC) from multidimensional perspectives, covering chemotherapy, targeted therapy, immunotherapy, and radiotherapy. Accumulating evidence demonstrates that distinct cancer therapies induce heterogeneous cardiotoxic phenotypes, such as heart failure (HF), arrhythmia, and myocardial infarction (MI). There are some common mechanisms of CTIC, including oxidative stress (OS) and mitochondrial dysfunction, while immune checkpoint inhibitors demonstrate unique immune-related mechanisms that lead to cardiotoxicity. In terms of biomarkers, troponins, natriuretic peptides, soluble suppression of tumorigenicity 2 receptor, galectin-3, myeloperoxidase, matrix metalloproteinases, growth differentiation factor-15, and some single-nucleotide polymorphisms, microRNAs, and inflammatory cytokines provide a basis for early diagnosis of CTIC. PS exacerbates CTIC through excessive activation of the sympathetic nervous system, disrupting the hypothalamic-pituitary-adrenal axis, unbalancing the immune-inflammatory response, and inducing OS and mitochondrial dysfunction. The treatment strategies for CTIC mainly include natural products, nano-targeted drugs, and combination therapies. In addition, special populations, such as pediatric and elderly patients, require tailored strategies due to their unique vulnerabilities. Overall, this review summarizes the characteristics, mechanisms, biomarkers, PS effects, and progress in therapy for CTIC, providing a multidimensional frame for early clinical diagnosis and intervention in CTIC. Future directions involve integrating multi-omics, digital health, and personalized interventions to improve CTIC management, highlighting the need for interdisciplinary collaboration between oncology and cardiology.