Review Article
2020 Dec 18;105383.
JOURNAL：Pharmacol Res.
Article Link
Endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity may be therapeutically targeted by natural and chemical compounds: A review
F Yarmohammadi, R Rezaee, AW Haye et al.
KEYWORDS
apoptosis; autophagy; cardiac damage; doxorubicin; inflammation
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.
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