Cardiac fibrosis in oncologic therapies

Cardiotoxicity, or the development of unwarranted cardiovascular side-effects of oncologic therapies, can involve all aspects of cardiovascular disease. The development of cardiac fibrosis is a dreaded complication that leads to cardiac mechanical dysfunction, tachyarrhythmias, and an increase in cardiovascular mortality. This review details established and putative mechanisms, leading to fibroblast activation, myofibroblast transdifferentiation, and the development of replacement or interstitial cardiac fibrosis as a consequence of cancer treatments. Clinical and imaging strategies for cardiac fibrosis assessment as well as emerging antifibrotic therapeutics will also be addressed.

Automated summary

Cardiotoxicity, a potential side-effect of oncologic therapies, can lead to the development of cardiac fibrosis, which increases the risk of cardiac dysfunction and cardiovascular mortality. This review focuses on the mechanisms of fibroblast activation, myofibroblast transdifferentiation, and the development of cardiac fibrosis as a consequence of cancer treatments. It also discusses clinical strategies for assessing cardiac fibrosis and emerging therapies to prevent or treat fibrosis.