Mechanisms shared between cancer, heart failure, and targeted anti-cancer therapies

Sanne de Wit, Claire Glen, Rudolf A. de Boer, Ninian N. Lang

Research output: Contribution to journalReview articleAcademicpeer-review

1 Citation (Scopus)

Abstract

Heart failure (HF) and cancer are the leading causes of death worldwide and accumulating evidence demonstrates that HF and cancer affect one another in a bidirectional way. Patients with HF are at increased risk for developing cancer, and HF is associated with accelerated tumour growth. The presence of malignancy may induce systemic metabolic, inflammatory, and microbial alterations resulting in impaired cardiac function. In addition to pathophysiologic mechanisms that are shared between cancer and HF, overlaps also exist between pathways required for normal cardiac physiology and for tumour growth. Therefore, these overlaps may also explain the increased risk for cardiotoxicity and HF as a result of targeted anti-cancer therapies. This review provides an overview of mechanisms involved in the bidirectional connection between HF and cancer, specifically focusing upon current 'hot-topics' in these shared mechanisms. It subsequently describes targeted anti-cancer therapies with cardiotoxic potential as a result of overlap between their anti-cancer targets and pathways required for normal cardiac function.

Original languageEnglish
Pages (from-to)3451-3466
Number of pages16
JournalCardiovascular Research
Volume118
Issue number18
DOIs
Publication statusPublished - 3 Feb 2023
Externally publishedYes

Bibliographical note

Publisher Copyright:
© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

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