Effect of TGFB1 and Smad3 deficiency on doxorubicin cardiotoxity

To examine the role of the TGF-beta/Smad3 pathway in cardiac damage by doxorubicin, we performed comparitive RNA sequencing analysis of human cardiac endothelial cells transfected with Smad3 shRNA Overall design: To determine if the endothelial response to TGF-beta1 was enhanced by pretreatment with doxorubicin, human cardiac endothelial cells were pretreated with doxorubicin and subsequently exposed to TGF-beta1 to examine activation of the canonical pathway.