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

被引:12
|
作者
de Wit, Sanne [1 ]
Glen, Claire [2 ]
de Boer, Rudolf A. [1 ]
Lang, Ninian N. [2 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, POB 30-001,Hanzepl 1, NL-9700 RB Groningen, Netherlands
[2] Univ Glasgow, Inst Cardiovasc & Med Sci, 126 Univ Pl, Glasgow G12 8TA, Lanark, Scotland
基金
欧洲研究理事会;
关键词
Cancer; Heart failure; Cardiotoxic drugs; Mechanisms; TRIMETHYLAMINE-N-OXIDE; ENDOTHELIAL GROWTH-FACTOR; PROMOTES TUMOR-GROWTH; INDUCIBLE FACTOR-I; BODY-MASS INDEX; CLONAL HEMATOPOIESIS; COLORECTAL-CANCER; GUT MICROBIOME; INCREASED RISK; CELL-GROWTH;
D O I
10.1093/cvr/cvac132
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:3451 / 3466
页数:16
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