Role of non-cardiomyocytes in anticancer drug-induced cardiotoxicity: A systematic review

Cardiotoxicity induced by anticancer drugs interferes with the continuation of optimal treatment, inducing life-threatening risks or leading to long-term morbidity. The heart is a complex pluricellular organ comprised of cardiomyocytes and non-cardiomyocytes. Although the study of these cell populations has been often focusing on cardiomyocytes, the contributions of non-cardiomyocytes to development and disease are increasingly being appreciated as both dynamic and essential. This review summarized the role of non-cardiomyocytes in anticancer drug-induced cardiotoxicity, including the mechanism of direct damage to resident non-cardiomyocytes, cardiomyocytes injury caused by paracrine modality, myocardial inflammation induced by transient cell populations and the protective agents that focused on non-cardiomyocytes.

Automated summary

Cardiotoxicity caused by anticancer drugs can pose life-threatening risks or long-term morbidity by interfering with optimal treatment. The heart is a complex organ composed of cardiomyocytes and non-cardiomyocytes, with non-cardiomyocytes playing an increasingly recognized dynamic and essential role in drug-induced cardiotoxicity. This review provides an overview of the involvement of non-cardiomyocytes in cardiotoxicity, including direct damage, paracrine-induced cardiomyocyte injury, transient cell-induced myocardial inflammation, and protective agents targeting non-cardiomyocytes.