Key result
Novel cancer therapeutics can cause chemotherapy-induced heart failure by targeting pathways involved in the cardiovascular system, necessitating an understanding of the underlying molecular mechanisms.
Why the study?
Novel cancer therapeutics can target pathways involved in the cardiovascular system and cause chemotherapy-induced heart failure, limiting their applicability and worsening long-term morbidity and mortality.
This review highlights the molecular mechanisms of chemotherapy-induced heart failure from novel cancer therapeutics and discusses clinical management strategies.
Raises caution for cardiotoxicity limiting novel cancer therapies; leaves open optimal monitoring and prevention in survivors.
Novel cancer therapeutics contribute to a steadily declining cancer mortality. However, several of these new therapies target pathways also involved in the cardiovascular system thus causing cardiotoxic side effects such as chemotherapy-induced heart failure (CIHF). This might limit the applicability of these effective treatments in a relevant number of patients. Furthermore, given the improving cancer survival rates, chemotherapy-induced cardiotoxic complications receive increasing attention given their potential impact on long-term morbidity and mortality. The understanding of molecular mechanisms that underlie CIHF is crucial for future improvement of pharmacodynamics of these therapeutics but also for developing specific interventions to prevent CIHF. Here, we discuss molecular mechanisms underlying CIHF of novel cancer therapeutics including a short synopsis on clinical management of patients suffering from CIHF.
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Braumann et al. (2018) conducted a review in Chemotherapy-induced heart failure. Novel cancer therapeutics was evaluated. Novel cancer therapeutics can cause chemotherapy-induced heart failure by targeting pathways involved in the cardiovascular system, necessitating an understanding of the underlying molecular mechanisms.
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