Effect of DGK-zeta-overexpression on doxorubicin-induced cardiotoxicity in mice.

Doxorubicin (Dox)-induced cardiotoxicity is still an important medical problem associated with a high mortality rate in cancer survivors. p53 plays a key role in Dox-induced cardiotoxicity. Diacylglycerol kinase zeta (Dgk-zeta) regulates the p53 protein expression level in neurons. However, it has not been clarified whether Dgk-zeta regulates p53 in the development of Dox-induced cardiomyopathy. To investigate the functional role of Dgk-zeta in Dox-induced cardiotoxicity, we generated cardiac-specific overexpression of Dgk-zeta transgenic mice and injected Dox to them and wild-type littermates.