This review summarizes the intracellular signaling pathways and membrane transporter interactions involved in TKI-induced cardiotoxicity, alongside recent methodological advances to study its etiology.
Understanding the interaction of TKIs with cardiac cell membrane transporters and intracellular signaling pathways is crucial for elucidating the mechanisms of TKI-induced cardiotoxicity.
Tyrosine kinase inhibitors (TKIs) are a class of drugs that have significantly improved survival outcomes and revolutionized the treatment landscape for cancer patients. This is due to their ability to suppress the dysregulation of phosphorylation targets contributing to tumor progression, however, many TKIs approved to treat cancer are associated with adverse cardiac events, including potentially lethal cardiotoxicity. Despite extensive research on kinase signaling pathways, the mechanisms that regulate the movement of TKIs across cardiac cell membranes to interfere with the targets associated with TKI-induced cardiotoxicity remains to be fully elucidated. In this review, we focus on 1) summarizing the purported intracellular signaling pathways associated with TKI-induced cardiotoxicity, 2) the interaction of TKIs with membrane transporters, and 3) recent technological and methodological advances that can be leveraged to study the role of membrane transporters in the etiology of TKI-induced cardiotoxicity.
Xu et al. (Wed,) conducted a review in TKI-induced cardiotoxicity. Tyrosine kinase inhibitors (TKIs) was evaluated. This review summarizes the intracellular signaling pathways and membrane transporter interactions involved in TKI-induced cardiotoxicity, alongside recent methodological advances to study its etiology.