PRMT1 suppresses doxorubicin-induced cardiotoxicity by inhibiting endoplasmic reticulum stress.

Doxorubicin (Dox) is a widely used anti-cancer drug that has a significant limitation, which is cardiotoxicity. Its cardiotoxic side effect is dose dependent and occurs through any age. Dox has been known to exert its toxic effect through oxidative stress, but an emerging mechanism is endoplasmic reticulum (ER) stress that activates proapoptotic pathway involving PERK/ATF4/CHOP axis.