ABSTRACT
Doxorubicin (DOX) is a chemotherapeutic agent with marked,
dose-dependent cardiotoxicity that leads to tachycardia, atrial and
ventricular arrhythmia, and irreversible heart failure. Induction of the
endoplasmic reticulum (ER) which plays a major role in protein folding
and calcium homeostasis was reported as a key contributor to cardiac
complications of DOX. This article reviews several chemical compounds
that have been shown to regulate DOX-induced inflammation, apoptosis,
and autophagy via inhibition of ER stress signaling pathways, such as
the IRE1α/ASK1/JNK, IRE1α/JNK/Beclin-1, and CHOP pathways.