Characterization of the molecular mechanisms underlying sunitinib-induced cardiotoxicity via autophagy manipulated MYLK3 degradation

Sunitinib, which is a kind of tyrosine kinases that can selectively target multiple receptors, exhibits antiangiogenic and antitumor activity, and extends survival of patients with metastatic renal-cell carcinoma (mRCC) and gastrointestinal stromal tumors (GIST). This molecule has also been reported to be associated with cardiotoxicity at a high frequency, including hypertension, electrocardiogram (ECG) changes, reduction of left ventricular ejection fraction (LVEF), and heart failure.