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

Doxorubicin (DOX), an effective chemotherapeutic drug for various cancers, has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell (EC) dysfunction is recognized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. Transcription factor EB (TFEB), a master autophagy regulator, regulates cardiovascular homeostasis. In the present study, we aimed to test whether endothelial TFEB protects against EC damage after DOX treatment. Overall design: Total RNA was extracted from HUVECs stably overexpressing sfGFP-TFEB or empty vector after treatment with vehicle or DOX (1 uM) for 24 hours. RNA sequencing analysis was performed in empty vector and TFEB stable expressing ECs with or without DOX treatment.