Cancer therapy-induced cardiotoxicity is driven by oxidative stress and mitochondrial dysfunction, exacerbated by psychological stress, and managed with natural products and nano-targeted drugs.
This comprehensive review outlines the mechanisms, biomarkers, and management strategies for cancer therapy-induced cardiotoxicity, highlighting the exacerbating role of psychological stress.
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 excessively activating 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. • Oxidative stress and mitochondrial dysfunction are the common mechanisms of cancer therapy-induced cardiotoxicity (CTIC). • There are ten main biomarkers of CTIC. • Psychological stress (PS) exacerbates CTIC through multiple pathways. • Natural products, nano-targeted drugs, and combination therapies have mainly been used to treat CTIC.
Chen et al. (Mon,) conducted a review in Cancer therapy-induced cardiotoxicity. Cancer therapy was evaluated. Cancer therapy-induced cardiotoxicity is driven by oxidative stress and mitochondrial dysfunction, exacerbated by psychological stress, and managed with natural products and nano-targeted drugs.
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