Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies.

ABSTRACT:

Aims

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myelogenous leukaemia (CML). However, cardiotoxicity of these agents remains a serious concern. The underlying mechanism of these adverse cardiac effects is largely unknown. Delineation of the underlying mechanisms of TKIs associated cardiac dysfunction could guide potential prevention strategies, rescue approaches, and future drug design. This study aimed to determine the cardiotoxic potential of approved CML TKIs, define the associated signalling mechanism and identify potential alternatives.

Methods and results

In this study, we employed a zebrafish transgenic BNP reporter line that expresses luciferase under control of the nppb promoter (nppb:F-Luciferase) to assess the cardiotoxicity of

SUBMITTER: Singh AP 

PROVIDER: S-EPMC6452321 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature