Does rac1 signalling mediate doxorubicin-induced cardiotoxicity through both reactive oxygen species-dependent and -independent pathways?
Rac1 signalling contributes to doxorubicin-induced cardiotoxicity through both a ROS-dependent mechanism and ROS-independent HDAC/p53 signalling in cardiomyocytes. Thus, inhibition of Rac1 may be a useful therapy for doxorubicin-induced cardiotoxicity.
Long noncoding RNA TUC338 overexpression leads to enhanced proliferation and reduced apoptosis in TSCC.