p38 delta systemic genetic deletion mitigates anthracycline cardiotoxicity in female mice

Doxorubicin (DOX) is an effective anthracycline chemotherapy, but its clinical use is limited by dose-dependent cardiotoxicity. We previously found that systemic genetic deletion of the p38δ kinase protects female mice from DOX-induced cardiotoxicity (DIC), suggesting that selective inhibition of this kinase may be a therapeutic strategy. To explore the mechanisms underlying this protection, we performed bulk RNA sequencing to profile transcriptomic changes associated with p38δ deletion during DIC.