Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Doxorubicin (DOX) has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell dysfunction is recoginized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. Endothelial TFEB protects against EC damage and cardiac dysfunction. Cardiac single cells isolated from vehicle and doxorubicin treated wild type and EC-Tfeb Tg mice were collected for scRNA-seq analysis. Overall design: Mouse heart tissues from male EC-Tfeb Tg mice and WT mice treated with DOX (5 mg/kg, iv, once a week) or vehicle for 2 weeks (n = 4-5 / group). Cardiac single cells isolated from wild type and EC-Tfeb Tg mice treated with vehicle or doxorubicin were collected for scRNA-seq analysis.