TY  - JOUR
ID  - enlighten275583
UR  - https://eprints.gla.ac.uk/275583/
IS  - 8
A1  - de Wit, Sanne
A1  - Glen, Claire
A1  - de Boer, Rudolf A.
A1  - Lang, Ninian N.
N2  - 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.
VL  - 118
TI  - Mechanisms shared between cancer, heart failure, and targeted anti-cancer therapies
AV  - public
EP  - 3466
N1  - NNL is supported by a British Heart Foundation Centre of Research Excellence Grant (RE/18/6/34217). RAdB is supported by by the European Research Council (ERC CoG 818715); by the Netherlands Heart Foundation (grants 2017-21; 2017-11; 2018-30; 2020B005), by the leDucq Foundation (Cure-PLaN).
Y1  - 2022/12//
PB  - Oxford University Press
JF  - Cardiovascular Research
SN  - 0008-6363
SP  - 3451
ER  -