Ponatinib-induced cardiotoxicity is driven by S100A8/A9-NLRP3-IL-1β signaling mediated excessive inflammation

To delineate the underlying molecular mechanisms of ponatinib-induced cardiotoxicity, we used we a comorbitity cardiotoxicity mouse model (high fat-fed ApoE-/- mice) treated for two weeks with placebo/ or Ponatinib We then performed gene expression profiling analysis on left ventricular tissues from the two mouse groups Comparative gene expression profiling analysis of RNA-seq data for Placebo or Ponatinib-treated high fat-fed ApoE-/- mice